Search

Your search keyword '"C. Storelli"' showing total 204 results
Start Over Author "C. Storelli"
204 results on '"C. Storelli"'

1. Poster session 2Morphogenetic mechanisms290MiR-133 regulates retinoic acid pathway during early cardiac chamber specification291Bmp2 regulates atrial differentiation through miR-130 during early heart looping formationDevelopmental genetics294Association of deletion allele of insertion/deletion polymorphism in alpha 2B adrenoceptor gene and hypertension with or without type 2 diabetes mellitus295Association of G1359A polymorphism of the endocannabinoid type 1 receptor (CNR1) with coronary artery disease (CAD) with type 2 diabetes mellitusCell growth, differentiation and stem cells - Vascular298Gamma-secretase inhibitor prevents proliferation and migration of ductus arteriosus smooth muscle cells: a role of Notch signaling in postnatal closure of ductus arteriosus299Mesenchymal stromal-like cells (MLCs) derived from induced pluripotent stem (iPS) cells: a promising therapeutic option to promote neovascularization300Sonic Hedgehog promotes mesenchymal stem cell differentiation to vascular smooth muscle cells in cardiovacsular disease301Proinflammatory cytokine secretion and epigenetic modification in endothelial cells treated LPS-GinfivalisCell death and apoptosis - Vascular304Mitophagy acts as a safeguard mechanism against human vascular smooth muscle cell apoptosis induced by atherogenic lipidsTranscriptional control and RNA species - Vascular307MicroRNA-34a role in vascular calcification308Local delivery of a miR-146a inhibitor utilizing a clinically applicable approach attenuates neointima formation after vascular injury309Long noncoding RNA landscape of hypoxic endothelial cells310Specific circulating microRNAs levels associate with hypertension, hyperglycemia and dysfunctional HDL in acute coronary syndrome patientsCytokines and cellular inflammation - Vascular313Phosphodiesterase5A up-regulation in vascular endothelium under pro-inflammatory conditions: a newly disclosed anti-inflammatory activity for the omega-3polyunsaturated aatty acid docosahexaenoic acid314Cardiovascular risk modifying with extra-low dose anticytokine drugs in rhematoid arthritis315Conversion of human M-CSF macrophages into foam cells reduces their proinflammatory responses to classical M1-polarizing activation316Lymphocytic myocarditis coincides with increased plaque inflammation and plaque hemorrhage in coronary arteries, facilitating myocardial infarction317Serum osteoprotegerin level predictsdeclined numerous of circulating endothelial- derived and mononuclear-derived progenitor cells in patients with metabolic syndromeGrowth factors and neurohormones - Vascular320Effect of gastrin-releasing peptide (GRP) on vascular inflammationSignal transduction - Heart323A new synthetic peptide regulates hypertrophy in vitro through means of the inhibition of nfkb324Inducible fibroblast-specific knockout of p38 alpha map kinase is cardioprotective in a mouse model of isoproterenol-induced cardiac hypertrophy325Regulation of beta-adrenoceptor-evoked inotropic responses by inhibitory G protein, adenylyl cyclase isoforms 5 and 6 and phosphodiesterases326Binding to RGS3 and stimulation of M2 muscarinic acetylcholine receptors modulates the substrate specificity of p190RhoGAP in cardiac myocytes327Cardiac regulation of post-translational modifications, parylation and deacetylation in LMNA dilated cardiomyopathy mouse model328Beta-adrenergic regulation of the b56delta/pp2a holoenzyme in cardiac myocytes through b56delta phosphorylation at serine 573Nitric oxide and reactive oxygen species - Vascular331Oxidative stress-induced miR-200c disrupts the regulatory loop among SIRT1, FOXO1 and eNOS332Antioxidant therapy prevents oxidative stress-induced endothelial dysfunction and Enhances Wound Healing333Morphological and biochemical characterization of red blood cell in coronary artery diseaseCytoskeleton and mechanotransduction - Heart336Novel myosin activator, JSH compounds, increased myocardial contractility without chronotropic effect in ratsExtracellular matrix and fibrosis - Vascular339Ablation of Toll-like receptor 9 causes cardiac rupture after myocardial infarction by attenuating proliferation and differentiation of cardiac fibroblasts340Altered vascular remodeling in the mouse hind limb ischemia model in Factor VII activating protease (FSAP) deficiencyVasculogenesis, angiogenesis and arteriogenesis343Pro-angiogenic effects of proly-hydroxylase inhibitors and their potential for use in a novel strategy of therapeutic angiogenesis for coronary total occlusion344Nrf2 drives angiogenesis in transcription-independent manner: new function of the master regulator of oxidative stress response345Angiogenic gene therapy, despite efficient vascular growth, is not able to improve muscle function in normoxic or chronically ischemic rabbit hindlimbs -role of capillary arterialization and shunting346Effect of PAR-1 inhibition on collateral vessel growth in the murine hind limb model347Quaking is a key regulator of endothelial cell differentiation, neovascularization and angiogenesis348'Emerging angiogenesis' in the chick chorioallantoic membrane (CAM). An in vivo study349Exosomes from cardiomyocyte progenitor cells and mesenchymal stem cells stimulate angiogenesis in vitro and in vivo via EMMPRINEndothelium352Reciprocal regulation of GRK2 and bradykinin receptor stimulation modulate Ca2+ intracellular level in endothelial cells353The roles of bone morphogenetic proteins 9 and 10 in endothelial inflammation and atherosclerosis354The contribution of GPR55 to the L-alpha-lysophosphatidylinositol-induced vasorelaxation in isolated human pulmonary arteries355The endothelial protective ACE inhibitor Zofenoprilat exerts anti-inflammatory activities through H2S production356A new class of glycomimetic drugs to prevent free fatty acid-induced endothelial dysfunction357Endothelial progenitor cells to apoptotic endothelial cell-derived microparticles ration differentiatesas preserved from reduced ejection fractionheart failure358Proosteogenic genes are activated in endothelial cells of patients with thoracic aortic aneurysm359Endothelin ETB receptors mediate relaxing responses to insulin in pericardial resistance arteries from patients with cardiovascular disease (CVD)Smooth muscle and pericytes362CX3CR1 positive myeloid cells regulate vascular smooth muscle tone by inducing calcium oscillations via activation of IP3 receptors363A novel function of PI3Kg on cAMP regulation, role in arterial wall hyperplasia through modulation of smooth muscle cells proliferation364NRP1 and NRP2 play important roles in the development of neointimal hyperplasia in vivo365Azithromycin induces autophagy in aortic smooth muscle cellsCoagulation, thrombosis and platelets368The real time in vivo evaluation of platelet-dependent aldosterone prothrombotic action in mice369Development of a method for in vivo detection of active thrombi in mice370The antiplatelet effects of structural analogs of the taurine chloramine371The influence of heparin anticoagulant drugs on functional state of human platelets372Regulation of platelet aggregation and adenosine diphosphate release by d dimer in acute coronary syndrome (in vitro study)Oxygen sensing, ischaemia and reperfusion375Sirtuin 5 mediates brain injury in a mouse model of cerebral ischemia-reperfusion376Abscisic acid: a new player in cardiomyocyte protection from ischaemia?377Protective effects of ultramicronized palmitoylethanolamide (PEA-um) in myocardial ischaemia and reperfusion injury in vivo378Identification of stem cell-derived cardiomyocytes using cardiac specific markers and additional testing of these cells in simulated ischemia/reperfusion system379Single-dose intravenous metformin treatment could afford significant protection of the injured rat kidney in an experimental model of ischemia-reperfusion380Cardiotoxicity of long acting muscarinic receptor antagonists used for chronic obstructive pulmonary disease381Dependence antioxidant potential on the concentration of amino acids382The impact of ischemia-reperfusion on physiological parameters,apoptosis and ultrastructure of rabbit myocardium with experimental aterosclerosisMitochondria and energetics385MicroRNA-1 dependent regulation of mitochondrial calcium uniporter (MCU) in normal and hypertrophied hearts386Mitochondrial homeostasis and cardioprotection: common targets for desmin and aB-crystallin387Overexpression of mitofusin-2 (Mfn2) and associated mitochondrial dysfunction in the diabetic heart388NO-dependent prevention of permeability transition pore (MPTP) opening by H2S and its regulation of Ca2+ accumulation in rat heart mitochondria389G protein coupled receptor kinase 2 (GRK2) is fundamental in recovering mitochondrial morphology and function after exposure to ionizing radiation (IR)Gender issues392Sex differences in pulmonary vascular control; focus on the nitric oxide pathwayAging395Heart failure with preserved ejection fraction develops when feeding western diet to senescence-accelerated mice396Cardiovascular markers as predictors of cognitive decline in elderly hypertensive patients397Changes in connexin43 in old rats with volume overload chronic heart failureGenetics and epigenetics400Calcium content in the aortic valve is associated with 1G>2G matrix metalloproteinase 1 polymorphism401Neuropeptide receptor gene s (NPSR1) polymorphism and sleep disturbances402Endothelin-1 gene Lys198Asn polymorphism in men with essential hypertension complicated and uncomplicated with chronic heart failure403Association of common polymorphisms of the lipoprotein lipase and pon1 genes with the metabolic syndrome in a sample of community participantsGenomics, proteomics, metabolomics, lipidomics and glycomics405Gene expression quantification using multiplexed color-coded probe pairs to determine RNA content in sporadic cardiac myxoma406Large-scale phosphorylation study of the type 2 diabetic heart subjected to ischemia / reperfusion injury407Transcriptome-based identification of new anti-inflammatory properties of the olive oil hydroxytyrosol in vascular endothelial cell under basal and proinflammatory conditions408Gene polymorphisms combinations and risk of myocardial infarctionComputer modelling, bioinformatics and big data411Comparison of the repolarization reserve in three state-of-the-art models of the human ventricular action potentialMetabolism, diabetes mellitus and obesity414Endothelial monocyte-activating polypeptide-II improves heart function in type -I Diabetes mellitus415Admission glucose level is independent predictor of impaired left ventricular function in patients with acute myocardial infarction: a two dimensional speckle-tracking echocardiography study416Association between biochemical markers of lipid profile and inflammatory reaction and stiffness of the vascular wall in hypertensive patients with abdominal obesity417Multiple common co-morbidities produce left ventricular diastolic dysfunction associated with coronary microvascular dysfunction, oxidative stress and myocardial stiffening418Investigating the cardiovascular effects of antiretroviral drugs in a lean and high fat/sucrose diet rat model of obesity419Statins in the treatment of non-alcoholic steatohepatitis (NASH). Our experience from a 2-year prospective study in Constanta County, Romania420Epicardial adipose tissue as a predictor of cardiovascular outcome in patients with ACS undergoing PCI?Arterial and pulmonary hypertension423Dependence between heart rhythm disorers and ID polymorphism of ACE gene in hypertensive patients424Molecular mechanisms underlying the beneficial effects of Urocortin 2 in pulmonary arterial hypertension425Inhibition of TGf-b axis and action of renin-angiotensin system in human ascending aorta aneurysms426Early signs of microcirculation and macrocirculation abnormalities in prehypertension427Vascular smooth muscle cell-expressed Tie-2 controls vascular tone428Cardiac and vascular remodelling in the development of chronic thrombo-embolic pulmonary hypertension in a novel swine modelBiomarkers431Arrhythmogenic cardiomyopathy: a new, non invasive biomarker432Can circulating microRNAs distinguish type 1 and type 2 myocardial infarction?433Design of a high-throughput multiplex proteomics assay to identify left ventricular diastolic dysfunction in diabetes434Monocyte-derived and P-selectin-carrying microparticles are differently modified by a low fat diet in patients with cardiovascular risk factors who will and who will not develop a cardiovascular event435Red blood cell distribution width assessment by polychromatic interference microscopy of thin films in chronic heart failure436Invasive and noninvasive evaluation of quality of radiofrequency-induced cardiac denervation in patients with atrial fibrillation437The effect of therapeutic hypothermia on the level of brain derived neurotrophic factor (BDNF) in sera following cardiopulmonary resustitation438Novel biomarkers to predict outcome in patients with heart failure and severe aortic stenosis439Biological factors linking depression and anxiety to cardiovascular disease440Troponins and myoglobin dynamic at coronary arteries graftingInvasive, non-invasive and molecular imaging443Diet composition effects on the genetic typing of the mouse ob mutation: a micro-ultrasound characterization of cardiac function, macro and micro circulation and liver steatosis444Characterization of pig coronary and rabbit aortic lesions using IV-OCT quantitative analysis: correlations with histologyGene therapy and cell therapy447Enhancing the survival and angiogenic potential of mouse atrial mesenchymal cells448VCAM-1 expression in experimental myocardial infarction and its relation to bone marrow-derived mononuclear cell retentionTissue engineering451Advanced multi layered scaffold that increases the maturity of stem cell-derived human cardiomyocytes452Response of engineered heart tissue to simulated ischemia/reperfusion in the presence of acute hyperglycemic conditions453Serum albumin hydrogels prevent de-differentiation of neonatal cardiomyocytes454A novel paintbrush technique for transfer of low viscosity ultraviolet light curable cyan methacrylate on saline immersed in-vitro sheep heart

Author

MC Arokiaraj, E J Humphrey, E Ruivo, P Benzoni, A Uitterdijk, S Malandraki-Miller, SJ Tarvainen, N Di Lascio, MA Charnaia, T Gegenava, N Sunderland, J Skopal, A Evtushenko, L Malinova, G Chiva-Blanch, J O'reilly, S Stojkovic, E Sommariva, K Stam, SS Kapel, M L Sasonko, L Borges, C Maia-Rocha, MV Krestjyaninov, M Tscharre, I R Parepa, A Genis, O Sorop, TI Petelina, CH Chimed, N A Dorofeyeva, M Paci, Y Timasheva, MA Carluccio, LE Smith, E L Stepien, R Prakaschandra, VM Zhebel, V Gafarov, GSB Guillermo Solache Berrocal, J Benes, A Noriega De La Colina, AB Gevaert, DPM De Wijs-Meijler, A Fiordelisi, A Budko, L Murfitt, A Diokmetzidou, G Borile, C R Revnic, A Korda, S Cassambai, B Medic, A Szantai, S Cuzzocrea, T Vigliarolo, C Diaz-Canestro, YM Roka-Moiia, M Murina, A Dickhout, A Gromotowicz, R Stamatiou, C Pellet-Many, A Lupieri, A Kumar, J G R De Mey, AS Kostina, A Berezin, FL Wilkinson, L Morbidelli, O Karpinska, CG Mitrofan, J Gambardella, JA Maring, W Rong, A Margariti, C Deffge, P Korpisalo, A Grochot-Przeczek, G A Barnett, J Herold, Y Omori, E-S Jeon, B Porro, A Orlandi, A Magenta, A Ranieri, N Vignier, M Levay, K Krobert, S A Bageghni, C Del Giudice, MK Bae, L Woudstra, F Da Silva, AR Babaeva, M Massaro, L S Niculescu, C Voellenkle, L Korte, I Badi, C Vindis, J Pizzicannella, Maryam Alshamrani, R Ferrer-Lorente, JH Hsu, W Hamed, C Lopez Sanchez, V Garcia-Martinez, D Franco, V Garcia-Lopez, A Aranega, C Lopez-Sanchez, S Tayel, H Khader, N El-Helbawy, A Alrefai, H El-Barbary, JR Wu, ZK Dai, JL Yeh, C Sanjurjo-Rodriguez, Y Richaud-Patin, FJ Blanco, L Badimon, A Raya, Paul A Cahill, F Diomede, I Merciaro, O Trubiani, H Nahapetyan, A Swiader, J Faccini, P Boya, M Elbaz, F Zeni, I Burba, M Bertolotti, MC Capogrossi, G Pompilio, A Raucci, R Widmer-Teske, J Dutzmann, J Bauersachs, K Donde, JM Daniel, DG Sedding, N Simionescu, GM Sanda, MG Carnuta, CS Stancu, AC Popescu, MR Popescu, A Vlad, DR Dimulescu, AV Sima, E Scoditti, M Pellegrino, N Calabriso, C Storelli, R De Caterina, KS Solodenkova, EV Kalinina, MN Usachiova, J Lappalainen, M DE C Lee-Rueckert, PT Kovanen, PS Biesbroek, RWE Emmens, AC Van Rossum, LJM Juffermans, JWM Niessen, PAJ Krijnen, A Kremzer, T Samura, T Berezina, E Gronenko, MK Kim, HJ Park, SK Bae, D Sorriento, M Ciccarelli, E Vernieri, P Campiglia, B Trimarco, G Iaccarino, K E Hemmings, K E Porter, J F Ainscough, M J Drinkhill, N A Turner, HG Hiis, MV Cosson, FO Levy, T Wieland, C Macquart, M Chatzifrangkeskou, A Evans, G Bonne, A Muchir, E Kemp, M Avkiran, F Carlomosti, M D'agostino, S Beji, G Zaccagnini, B Maimone, V Di Stefano, F De Santa, S Cordisco, A Antonini, R Ciarapica, E Dellambra, F Martelli, D Avitabile, MG Scioli, A Bielli, S Agostinelli, C Tarquini, V Tarallo, S De Falco, A Zaninoni, S Fiorelli, P Bianchi, G Teruzzi, I Squellerio, L Turnu, A Lualdi, E Tremoli, V Cavalca, YJ Lee, ES Ju, JO Choi, GY Lee, BK Lim, MANOJ Manickam, S-H Jung, S Omiya, K Otsu, S Nowak, M Wagner, RC Braun-Dullaeus, S Kostin, A Francke, S Subramaniam, SM Kanse, K Al-Lamee, CJ Schofield, S Egginton, AH Gershlick, D Kloska, A Kopacz, A Augustyniak, J Dulak, A Jozkowicz, J Hytonen, P Halonen, J Taavitsainen, S Tarvainen, T Hiltunen, T Liimatainen, K Kalliokoski, J Knuuti, S Yla-Herttuala, S Weinert, B Isermann, J Lee, A Cochrane, S Kelaini, J Bojdo, M Vila Gonzalez, Y Hu, D Grieve, A W Stitt, L Zeng, Q Xu, B Reglin, W Xiang, B Nitzsche, M Maibier, AR Pries, KR Vrijsen, SAJ Chamuleau, V Verhage, CHG Metz, K Lodder, ECM Van Eeuwijk, SM Van Dommelen, PA Doevendans, AM Smits, MJ Goumans, JPG Sluijter, M Bova, S Loffredo, S Appleby, N Morrell, M Baranowska-Kuczko, M Kloza, E Ambrozewicz, M Kozlowski, B Malinowska, H Kozlowska, M Monti, E Terzuoli, M Ziche, AM Mahmoud, AM Jones, JA Wilkinson, M Romero, J Duarte, MY Alexander, G Faggian, AA Kostareva, AB Malashicheva, TM Leurgans, TN Nguyen, A Irmukhamedov, LP Riber, R Mcgeogh, S Comer, A Blanco Fernandez, A Ghigo, R Blaise, NF Smirnova, N Malet, P Vincent, I Limon, S Gayral, E Hirsch, M Laffargue, V Mehta, I Zachary, I Aidonidis, K Kramkowski, W Miltyk, P Kolodziejczyk, A Gradzka, J Szemraj, E Chabielska, I Dijkgraaf, N Bitsch, S Van Hoof, F Verhaegen, R Koenen, TM Hackeng, D I Roshchupkin, K V Buravleva, VI Sergienko, DD Zhernossekov, VM Rybachuk, TV Grinenko, N Furman, P Dolotovskaya, M Shamyunov, T Denisova, M Reiner, A Akhmedov, S Keller, M Miranda, S Briand, L Barile, G Kullak-Ublick, T Luscher, G Camici, L Guida, M Magnone, P Ameri, E Lazzarini, C Fresia, S Bruzzone, E Zocchi, R Di Paola, M Cordaro, R Crupi, R Siracusa, M Campolo, G Bruschetta, R Fusco, P Pugliatti, E Esposito, J Paloczi, R Gaspar, A Dinnyes, J Kobolak, P Ferdinandy, A Gorbe, Z Todorovic, D Krstic, K Savic Vujovic, D Jovicic, G Basta Jovanovic, S Radojevic Skodric, M Prostran, S Dean, CJ Mee, KL Harvey, A Hussain, C Pena, B Paltineanu, S Voinea, F Revnic, C Ginghina, T Zaglia, P Ceriotti, A Campo, P Carullo, A Armani, R Coppini, V Vida, I Olivotto, G Stellin, R Rizzuto, D De Stefani, M Sandri, D Catalucci, M Mongillo, E Soumaka, I Kloukina, M Tsikitis, M Makridakis, A Varela, C Davos, A Vlachou, Y Capetanaki, MM Iqbal, H Bennett, B Davenport, C Pinali, G Cooper, E Cartwright, A Kitmitto, NA Strutynska, LA Mys, VF Sagach, A Franco, A Verzijl, R Van Duin, IKM Reiss, DJ Duncker, D Merkus, H Shakeri, M Orije, AJ Leloup, CE Van Hove, EM Van Craenenbroeck, GRY De Meyer, CJ Vrints, K Lemmens, L Desjardins-Creapeau, R Wu, M Lamarre-Cliche, P Larochelle, L Bherer, H Girouard, M Melenovsky, A Kvasilova, K Ruskova, D Sedmera, ABV Ana Barral, M Martin Fernandez, PRG Pablo Roman Garcia, JCLL Juan Carlos Llosa, MND Manuel Naves Diaz, CM Cesar Moris, JBCA Jorge B Cannata-Andia, IR Isabel Rodriguez, M Voevoda, E Gromova, V Maximov, D Panov, I Gagulin, A Gafarova, H Palahniuk, IP Pashkova, NV Zhebel, OL Starzhynska, DP Naidoo, K Rawojc, F J Enguita, G Grudzien, SJ Cordwell, MY White, R Martinelli, V Gatta, TR Nasibullin, VV Erdman, IA Tuktarova, OE Mustafina, J Hyttinen, S Severi, GG Vorobyov, KH Batmyagmar, Z Lkhagvasuren, LI Gapon, NA Musikhina, KS Avdeeva, SM Dyachkov, I Heinonen, M Van Kranenburg, VJ De Beer, Y Octavia, RJ Van Geuns, AH Van Den Meiracker, J Van Der Velden, FP Everson, T Ogundipe, T Grandjean, P De Boever, N Goswami, H Strijdom, A I Suceveanu, A P Suceveanu, L Mazilu, D E Tofoleanu, D Catrinoiu, M Rohla, C Hauser, K Huber, H Wojta, TW Weiss, MA Melnikova, NV Olezov, RH Gimaev, H Khalaf, VI Ruzov, R Adao, P Mendes-Ferreira, D Santos-Ribeiro, M Rademaker, AF Leite-Moreira, C Bras-Silva, LAA Alvarenga, RSP Falcao, RR Dias, S Lacchini, PS Gutierrez, JB Michel, YU I Gurfinkel, O YU Atkov, M Teichert, C Korn, C Mogler, S Hertel, C Arnold, T Korff, HG Augustin, RWB Van Duin, Y D'alessandra, F M Farina, M Casella, V Catto, C Carbucicchio, A Dello Russso, I Stadiotti, S Brambilla, M Chiesa, M Giacca, G I Colombo, C Tondo, F Ahlin, T Andric, D Tihanyi, J Wojta, E O'connell, A Butt, L Murphy, S Pennington, M Ledwidge, K Mcdonald, J Baugh, C Watson, R Suades, J Crespo, R Estruch, A Dyachenko, V Ryabukho, V Evtushenko, YU Saushkina, YU Lishmanov, K Smyshlyaev, A Bykov, S Popov, E Pavlyukova, Y Anfinogenova, E Szigetfu, B Kapornai, E Forizs, ZS Jenei, Z Nagy, B Merkely, E Zima, A Cai, R Dworakowski, T Gibbs, S Piper, N Jegard, T Mcdonagh, M Gegenava, II Dementieva, YUA Morozov, C Barsanti, F Stea, F Lenzarini, C Kusmic, F Faita, PJ Halonen, PH Puhakka, JP Hytonen, JM Taavitsainen, E A Supit, C A Carr, BCW Groenendijk, C Gorsse-Bakker, A Panasewicz, S Sneep, D Tempel, WJ Van Der Giessen, J Rys, C Daraio, P Dell'era, J Pigler, A Eder, T Eschenhagen, M M Mazo, N Amdursky, N S Peters, M M Stevens, and C M Terracciano

Subjects
chemistry.chemical_classification, Physiology, business.industry, Fatty acid, 030204 cardiovascular system & hematology, Pharmacology, medicine.disease, 03 medical and health sciences, 0302 clinical medicine, chemistry, Glycomimetic, Physiology (medical), medicine, Endothelial dysfunction, Cardiology and Cardiovascular Medicine, business, 030217 neurology & neurosurgery
Abstract

Background: Carbohydrates play a major role in cell signaling in many biological processes. We have developed a set of glycomimetic drugs that mimic the structure of carbohydrates and represent a novel source of therapeutics for endothelial dysfunction, a key initiating factor in cardiovascular complications. Purpose: Our objective was to determine the protective effects of small molecule glycomimetics against free fatty acid­induced endothelial dysfunction, focusing on nitric oxide (NO) and oxidative stress pathways. Methods: Four glycomimetics were synthesized by the stepwise transformation of 2,5­dihydroxybenzoic acid to a range of 2,5­substituted benzoic acid derivatives, incorporating the key sulfate groups to mimic the interactions of heparan sulfate. Endothelial function was assessed using acetylcholine­induced, endotheliumdependent relaxation in mouse thoracic aortic rings using wire myography. Human umbilical vein endothelial cell (HUVEC) behavior was evaluated in the presence or absence of the free fatty acid, palmitate, with or without glycomimetics (1µM). DAF­2 and H2DCF­DA assays were used to determine nitric oxide (NO) and reactive oxygen species (ROS) production, respectively. Lipid peroxidation colorimetric and antioxidant enzyme activity assays were also carried out. RT­PCR and western blotting were utilized to measure Akt, eNOS, Nrf­2, NQO­1 and HO­1 expression. Results: Ex vivo endothelium­dependent relaxation was significantly improved by the glycomimetics under palmitate­induced oxidative stress. In vitro studies showed that the glycomimetics protected HUVECs against the palmitate­induced oxidative stress and enhanced NO production. We demonstrate that the protective effects of pre­incubation with glycomimetics occurred via upregulation of Akt/eNOS signaling, activation of the Nrf2/ARE pathway, and suppression of ROS­induced lipid peroxidation. Conclusion: We have developed a novel set of small molecule glycomimetics that protect against free fatty acidinduced endothelial dysfunction and thus, represent a new category of therapeutic drugs to target endothelial damage, the first line of defense against cardiovascular disease.

Published
2016

2. Poster session 1

Author

J. Schlueter, T. Brand, D. J. Henderson, V. Boczonadi, P. Humbert, B. Chaudhry, D. Sedmera, J. Svatunkova, R. Kockova, B. Sankova, C. Lopez Sanchez, D. Franco, A. Aranega, V. Garcia-Martinez, E. Demina, V. Miroshikova, A. Denisenko, A. Schwarzman, F. Sanchez-Cabo, C. Torroja, A. Benguria, R. Buchan, P. Srivastava, F. Martinez, P. Barton, S. Cook, A. Dopazo, E. Lara-Pezzi, H. Rai, S. Kumar, A. K. Sharma, S. Mastana, A. Kapoor, C. M. Pandey, S. Agrawal, N. Sinha, J. Lipkova, M. Goldbergova, J. Parenica, J. Bienertova Vasku, A. Vasku, P. Kala, J. Spinar, L. Perez-Cabornero, D. Cantalapiedra, A. Forteza, R. Saez-Villaverde, J. Zumalde, V. Fernandez-Pedrosa, S. Zuniga-Trejos, M. Gil-Borja, M. Lazaro, S. Santillan, M. Costa, N. Cortez-Dias, P. Carrilho-Ferreira, D. Silva, C. Jorge, R. Placido, C. Calisto, M. Fiuza, A. Nunes Diogo, F. J. Enguita, H. H. W. Sillje, B. Lu, H. Yu, M. Zwartbol, W. P. Ruifrok, W. H. Van Gilst, R. A. De Boer, D. Zaliaduonyte-Peksiene, S. Simonyte, V. Lesauskaite, J. Vaskelyte, V. Mizariene, R. Zaliunas, W. Tigchelaar, E. Barlaka, A. Lazou, C. Del Giudice, E. Cipolletta, A. Anastasio, G. Santulli, M. Rusciano, A. S. Maione, P. Campiglia, M. Illario, B. Trimarco, G. Iaccarino, G. A. Frentzou, M. J. Drinkhill, N. A. Turner, S. G. Ball, J. F. X. Ainscough, L. Bertrand, F. Mailleux, J. Hammond, A. Ginion, L. Hue, J. L. Balligand, S. Horman, J. L. Vanoverschelde, C. Beauloye, B. Demeulder, S. L. Puhl, A. Mueller, Y. Devaux, D. R. Wagner, K. Roemer, M. Boehm, C. Maack, D. Miranda-Silva, I. Falcao-Pires, N. Goncalves, D. Moreira-Goncalves, A. F. Leite-Moreira, F. Mraiche, L. Fliegel, J. Xue, G. G. Haddad, L. C. Hsiao, C. Carr, Z. F. Cui, K. Clarke, M. A. D'amico, P. Izzicupo, A. Di Fonso, A. Bascelli, S. Gallina, A. Di Baldassarre, C. Silvestre, P. Fernandez, O. M. Pello, C. Indolfi, F. Civeira, R. Hutter, B. Ibanez, J. Chaves, J. Martinez-Gonzalez, V. Andres Garcia, A. Zabirnik, N. Smolina, A. Malashicheva, E. Omelchenko, T. Sejersen, A. Kostareva, C. Noack, M. P. Zafiriou, A. Renger, R. Dietz, H. J. Schaeffer, M. B. Bergmann, C. Zelarayan, S. Van Linthout, K. Miteva, M. P. Becher, M. Haag, J. Ringe, H.-P. schultheiss, M. Sittinger, C. Tschoepe, T. Kakuchaya, L. Bockeria, E. Golukhova, M. Eremeeva, N. Chigogidze, I. Aslanidi, I. Shurupova, A. Svobodov, A. A. Ramkisoensing, D. A. Pijnappels, J. Swildens, M. J. Goumans, M. J. Schalij, A. A. F. De Vries, D. E. Atsma, A. Gomes, G. M. Costa, C. A. Cordeiro, A. Matsuada, L. B. Rosario, A. P. Freire, M. Bousquenaud, M. Rolland-Turner, F. Maskali, L. Zhang, P. Y. Marie, F. Azuaje, A. J. Smith, G. M. Ellison, C. D. Waring, S. Purushothaman, D. Torella, B. Nadal-Ginard, M. H. Van Marion, D. W. J. Van Der Schaft, M.-J. Goumans, F. P. T. Baaijens, C. V. C. Bouten, N. Kraenkel, K. Kuschnerus, M. Mueller, T. Speer, S. Briand, M. Bader, P. Madeddu, T. F. Luescher, U. Landmesser, A. Papalamprou, C. Vicinanza, D. F. Goldspink, M. Noseda, S. J. Mcsweeney, T. Leja, E. Belian, I. Macaulay, F. Al-Beidh, S. Koenemann, M. S. Abreu Pavia, S. E. Jacobsen, M. D. Schneider, G. Foldes, Z. Bagyura, Z. Lendvai, D. Mathe, T. Nemeth, J. Skopal, I. Foldes, B. Merkely, S. E. Harding, A. J. Candasamy, R. S. Haworth, A. Boguslavsky, F. Cuello, M. J. Shattock, M. Mayr, M. Gautel, M. Avkiran, P. Leszek, B. Sochanowicz, M. Szperl, P. Kolsut, K. Brzoska, W. Piotrowski, T. Rywik, B. Danko, J. Rozanski, M. Kruszewski, N. Bouteldja, R. J. Woodman, C. L. Hewitson, E. Domingo, J. A. Barbara, A. A. Mangoni, R. Carnicer Hijazo, A. B. Hale, X. Liu, S. Suffredini, J. K. Bendall, G. B. S. Lim, N. J. Alp, K. M. Channon, B. Casadei, L. R. Moltzau, J. M. Aronsen, S. Meier, I. Sjaastad, T. Skomedal, J.-B. Osnes, F. O. Levy, E. Qvigstad, P. T. Wright, L. M. K. Pannell, A. R. Lyon, J. Gorelik, A. Guellich, S. F. Vatner, R. Fischmeister, B. Manoury, E. Dubois, J. Hamelet, A. Vanderper, P. Herijgers, D. Langin, F. Gartner, J. Gummert, H. Milting, G. Euler, M. Priess, J. Heger, T. Noll, R. Schulz, T. Doi, T. Akagami, T. Naka, T. Masuyama, M. Ohyanagi, M. Massaro, E. Scoditti, M. Pellegrino, M. A. Carluccio, C. Martines, C. Storelli, R. De Caterina, M. Falck-Hansen, M. E. Goddard, J. E. Cole, N. Astola, A. J. Cross, R. Krams, C. Monaco, M. F. Corsten, W. Verhesen, A. P. Papageorgiou, P. Carai, M. Lindow, S. Obad, G. Summer, L. De Rijck, S. Coort, M. Hazebroek, R. Van Leeuwen, M. Gijbels, M. P. J. De Winther, F. R. M. Stassen, S. Kauppinen, B. Schroen, S. Heymans, Z. Husti, V. Juhasz, L. Virag, A. Kristof, I. Koncz, T. Szel, I. Baczko, N. Jost, J. G. Y. Papp, A. Varro, A. Ghigo, A. Perino, F. Damilano, J. Leroy, V. O. Nikolaev, W. Richter, M. Conti, G. Vandecasteele, E. Hirsch, R. Ang, S. Sebastian, A. Ludwig, L. Birnbaumer, A. Tinker, E. A. Ertel, R. Sube, A. Opel, C. L-H Huang, A. Grace, N. Tribulova, J. Radosinska, B. Bacova, T. Benova, V. Knezl, J. Slezak, T. A. Matsuyama, T. Tanaka, T. Adachi, Y. Jiang, H. Ishibashi-Ueda, T. Takamatsu, J. Kornej, C. Reihardt, J. Kosiuk, A. Arya, G. Hindricks, V. Adams, D. Husser, A. Bollmann, S. Severi, M. Fantini, E. Ravagli, L. A. Charawi, D. Difrancesco, C. Poulet, L. Lu, U. R. Ravens, M. Hoch, T. Koenig, A. Gardiwal, B. Stapel, S. Erschow, A. Froese, B. Weinhold, R. Gerardy-Schahn, G. Klein, D. Hilfiker-Kleiner, K. Chinda, S. Palee, S. Surinkaew, M. Phornphutkul, S. Chattipakorn, N. Chattipakorn, B. Tuana, Z. Kohajda, A. A. Kristof, C. Corici, F. Fulop, N. L. Jost, V. Szuts, D. Menesi, G. L. Puskas, A. Zvara, N. Houshmand, J. G. Papp, N. Al-Shanti, M. Hancock, A. Venturini, C. Stewart, R. Ascione, G. Angelini, M.-S. Suleiman, A. Gonzalez-Tendero, I. Torre, F. Crispi, E. Gratacos, T. Tzanavari, E. Varela, A. Economides, S. Theocharis, C. Pantos, D. V. Cokkinos, A. Karalis, P. Hecker, V. Lionetti, W. C. Stanley, C. Ferrara, N. Piroddi, B. Scellini, C. Ferrantini, V. Sequiera, C. Remedios, L. Carrier, C. Tesi, J. Van Der Velden, C. Poggesi, V. Kooij, G. J. M. Stienen, D. Dooijes, s. Marston, C. Redwood, C. Dos Remedios, I. Diakonov, S. Tokar, M. Sikkel, S. Schlossarek, M. Sauer, A. Papageorgiou, S. Velthuis, E. Lutgens, M. Swinnen, N. Van Rooijen, J. Kzhyshkowska, P. Carmeliet, P. Garcia-Canadilla, F. Garcia-Garcia, I. Iruretagoiena, J. Dopazo, I. Amat-Roldan, M. H. Zhang, Y. H. Zhang, C. E. Sears, B. Wojtas, A. Llach, L. Hove-Madsen, V. Spinelli, L. Sartiani, M. Bucciantini, R. Coppini, E. Russo, A. Mugelli, E. Cerbai, M. Stefani, M. Ibrahim, P. Kukadia, M. Navaratnarajah, U. Siedlecka, C. Van Doorn, M. Yacoub, C. Terracciano, W. Song, N. Curtin, R. Woledge, S. Marston, M. Balteau, N. Tajeddine, G. Behets-Wydemans, C. Dessy, P. Gailly, W. J. Van Der Laarse, S. J. P. Bogaards, D. Van Groen, Y. Y. Wong, I. Schalij, A. Vonk Noordegraaf, F. M. Faz, B. Littlejohns, P. Pasdois, A. P. Halestrap, G. D. Angelini, S. Lemoine, V. Jaspard-Vinassa, F. Vigneron, P. Dos Santos, M. Popescu, A. Vlad, G. Isvoranu, L. Suciu, B. Marinescu, D. Dimulescu, L. Zagrean, P. W. M. Kleikers, K. Wingler, K. Radermacher, A. Sydykov, H. A. Ghofrani, N. Weissmann, H. H. W. Schmidt, A. Poddubnaya, K. E. M. Khurs, S. O. G. Smolenskaya, G. Szucs, Z. Murlasits, S. Torok, G. F. Kocsis, T. Csont, C. Csonka, P. Ferdinandy, R. Dongworth, D. M. Yellon, D. J. Hausenloy, Y. Y. Chen, W. S. Lian, C. F. Cheng, K. H. Khoo, T. C. Meng, G. Youcef, E. Belaidi, L. Fazal, M. P. Vinvent, D. De Paulis, G. Zadigue, C. Richer-Giudicelli, F. Alhenc-Gelas, M. Ovize, A. Pizard, R. Cal, J. Castellano, J. Farre, G. Vilahur, L. Badimon, V. Llorente-Cortes, H. Naz, M. Gharanei, C. Mee, H. Maddock, A. Hussain, O. Pisarenko, V. Shulzhenko, L. Serebryakova, I. Studneva, Y. Pelogeykina, D. Khatri, O. Tskitishvili, E. Barnucz, G. Veres, P. Hegedus, T. Radovits, S. Korkmaz, S. Klein, R. Zoller, M. Karck, G. Szabo, S. Morel, M. A. Frias, C. Rosker, R. W. James, S. Rohr, B. R. Kwak, V. Braunersreuther, B. Foglia, F. Mach, E. Shantsila, S. Montoro-Garcia, L. D. Tapp, S. Apostolakis, B. J. Wrigley, G. Y. H. Lip, E. Sokolowska, K. Przyborowski, K. Kramkowski, W. Buczko, A. Mogielnicki, U. Simonsen, E. R. Hedegaard, B. D. Nielsen, A. Kun, A. Hughes, C. Kroigaard, S. Mogensen, O. Frobert, K. Ait Aissa, J. P. Max, D. Wahl, T. Lecompte, P. Lacolley, V. Regnault, A. Novakovic, M. Pavlovic, A. Vranic, P. Milojevic, I. Stojanovic, M. Jovic, D. Nenezic, N. Ugresic, Q. Yang, G. W. He, L. Calvier, P. Reboul, B. Martin-Fernandez, V. Lahera, F. Zannad, V. Cachofeiro, P. Rossignol, N. Lopez-Andres, V. K. Pulakazhi Venu, R. Baetta, A. Bonomo, A. F. Muro, A. Corsini, A. L. Catapano, G. D. Norata, L. E. Viiri, L. E. Full, T. J. Navin, A. Didangelos, I. Seppala, T. Lehtimaki, A. H. Davies, R. Wait, D. Sedding, P. Stieger, C. Thoelen, S. Fischer, J. M. Daniel, R. Widmer-Teske, K. T. Preissner, N. Alenina, L. A. Rabelo, M. Todiras, V. N. Souza, J. M. Penninger, R. A. Santos, I. A. Leonova, S. A. Boldueva, V. S. Feoktistova, O. V. Sirotkina, M. G. Kolesnichenko, Z. Springo, P. Toth, P. Cseplo, G. Szijjarto, A. Koller, S. Puthenkalam, M. K. Frey, I. M. Lang, R. Madonna, H. Shelat, Y. J. Geng, T. Ziegler, V. Pfetsch, J. Horstkotte, C. Schwab, I. Rohwedde, R. Hinkel, Q. Di, S. Dietzel, U. Deutsch, C. Kupatt, I. Ernens, B. Lenoir, O. Fortunato, A. Caporali, E. Sangalli, D. Cordella, M. Marchetti, G. Spinetti, C. Emanueli, G. Arderiu, E. Pena, M. J. Forteza, V. Bodi, S. Novella, C. Alguero, I. Trapero, I. Benet, C. Hermenegildo, J. Sanchis, F. J. Chorro, A. Nemeth, S. Szabados, A. Cziraki, E. Sulyok, I. G. Horvath, M. Rauh, W. Rascher, I. Sikharulidze, I. B. Bakhlishvili, J. T. T. Laitinen, J. P. Hytonen, O. Leppanen, J. Taavitsainen, A. Partanen, P. Korpisalo, S. Yla-Herttuala, J. Lonn, J. Hallstrom, T. Bengtsson, M. C. Guisasola, E. Dulin, S. Stojkovic, C. Kaun, G. Maurer, K. Huber, J. Wojta, S. Demyanets, T. B. Opstad, A. Pettersen, S. Aakra, H. Arnesen, I. Seljeflot, M. Borrell-Pages, C. Romero, A. Toso, M. Leoncini, L. Tanini, T. Pizzetti, F. Tropeano, M. Maioli, P. Casprini, F. Bellandi, R. F. Antunes, J. C. Kaski, I. E. Dumitriu, E. Wu, A. A. L. Tareen, M. Udovychenko, I. Rudyk, K. Riches, L. Franklin, A. Maqbool, J. Bond, M. L. Koschinsky, D. J. O'regan, K. E. Porter, I. R. Parepa, A. I. Suceveanu, A. Suceveanu, L. Mazilu, L. Cojocaru, A. Rusali, L. A. Tuta, E. Craiu, D. Lindner, C. Zietsch, H.-P. Schultheiss, C. Tschope, D. Westermann, M. Miana, E. Martinez, R. Jurado, C. Delgado, N. Gomez-Hurtado, A. Briones, J. Young, T. J. Geng, A. Brodehl, T. Schmidt, O. Smolenskaya, C. Stegemann, D. Byzov, I. Mikhaylova, N. Chizh, E. Pushkova, O. Synchykova, B. Sandomirsky, O. Freylikhman, O. Rotar, N. Chromova, E. Moguchaya, V. Ivanenko, E. Kolesova, A. Erina, M. Boyarinova, A. Konradi, S. D. Preston, D. Baskaran, A. M. Plonczak, K. Norita, S. V. De Noronha, M. N. Sheppard, A. Haghikia, S. F. Hill, M. Hoepfner, B. Nitzsche, M. Schrader, F. Zengerling, B. Hoffmann, A. Pries, S. Gao, J. T. Laitinen, S. Laidinen, H. Markkanen, H. Karvinen, V. Marjomaki, I. Vajanto, T. T. Rissanen, K. Alitalo, P. Mello Ferrao, M. C. Waghabi, L. R. Garzoni, J. Ritterhoff, C. Weidenhammer, M. Voelkers, W. H. Zimmermann, J. Rabinowitz, P. Most, S. C. Gordts, I. Muthuramu, F. Jacobs, E. Van Craeyveld, E. Nefyodova, B. De Geest, D. R. Tribuddharat, D. R. Sathitkarnmanee, M. R. Buddhisa, M. S. Suwannasaen, D. R. Silarat, D. R. Ngamsangsirisup, D. R. Hawrylowicz, D. R. Lertmemongkolchai, S. Rain, M. L. Handoko, N. Westerhof, A. Vonk-Noordegraaf, F. S. De Man, A. S. Iakovleva, O. A. Mirolyubova, A. Berezin, T. A. Samura, Suwannasaen, Tippayawat, Ngamsangsirisup, D. R. Sutra, Hawrylowicz, Lertmemongkolchai, L. M. Lima, M. G. Carvalho, D. R. G. Junqueira, M. O. Sousa, A. Zampetaki, P. Willeit, L. Tilling, I. Drozdov, M. Prokopi, A. Shah, C. Boulanger, P. Chowienczyk, S. Kiechl, S. H. V. Oliveira, V. Kirillova, E. Prosviryakov, C. T. M. Van Der Pouw Kraan, F. J. P. Bernink, J. M. Baggen, L. Timmers, A. M. Beek, M. Diamant, A. C. Van Rossum, N. Van Royen, A. J. G. Horrevoets, J. E. A. Appelman, A. Zyatenkov, L. S. Kokov, Y. U. D. Volynskiy, M. Krestjyaninov, V. I. Ruzov, A. V. Villar, E. Martinez-Laorden, A. Almela, M. A. Hurle, M. L. Laorden, N. Apaijai, M. K. Mcmullen, J. M. Whitehouse, G. Shine, and A. Towell

Subjects
Gerontology, Physiology, business.industry, Physiology (medical), Cancer research, Medicine, SCRIB gene, Cardiology and Cardiovascular Medicine, business
Published
2012

3. Poster session 3

Author

O. Nanka, E. Krejci, Z. Pesevski, D. Sedmera, N. Smart, A. Rossdeutsch, K. N. Dube, J. Riegler, A. N. Price, A. Taylor, V. Muthurangu, M. Turner, M. F. Lythgoe, P. R. Riley, S. Kryvorot, T. Vladimirskaya, I. Shved, M. Schwarzl, S. Seiler, S. Huber, P. Steendijk, H. Maechler, M. Truschnig-Wilders, B. Pieske, H. Post, C. Caprio, A. Baldini, E. Chiavacci, L. Dolfi, L. Verduci, F. Meghini, F. Cremisi, L. Pitto, T.-C. Kuan, M.-C. Chen, T.-H. Yang, W.-T. Wu, C. S. Lin, H. Rai, S. Kumar, A. K. Sharma, S. Mastana, A. Kapoor, C. M. Pandey, S. Agrawal, N. Sinha, E. H. Orlowska-Baranowska, G. Placha, J. Gora, R. Baranowski, E. Abramczuk, T. Hryniewiecki, Z. Gaciong, J. J. W. Verschuren, J. A. M. Wessels, S. Trompet, D. J. Stott, N. Sattar, B. Buckley, H. J. Guchelaar, J. W. Jukema, M. Gharanei, A. Hussain, C. J. Mee, H. L. Maddock, W. J. Wijnen, S. Van Den Oever, I. Van Der Made, M. Hiller, A. J. Tijsen, Y. M. Pinto, E. E. Creemers, S. U. Y. Nikulina, A. Chernova, A. Petry, T. Rzymski, D. Kracun, F. Riess, L. Pike, A. L. Harris, A. Gorlach, R. Katare, A. Oikawa, F. Riu, A. P. Beltrami, D. Cesseli, C. Emanueli, P. Madeddu, T. Zaglia, G. Milan, M. Franzoso, P. Pesce, C. Sarais, M. Sandri, M. Mongillo, T. J. Butler, A.-M. L. Seymour, D. Ashford, F. Jaffre, M. Bussen, I. Flohrschutz, G. R. Martin, S. Engelhardt, G. Kararigas, B. T. Nguyen, H. Jarry, V. Regitz-Zagrosek, M. Van Bilsen, A. Daniels, C. Munts, B. J. A. Janssen, G. J. Van Der Vusse, F. A. Van Nieuwenhoven, C. Montalvo, A. V. Villar, D. Merino, R. Garcia, M. Llano, M. Ares, M. A. Hurle, J. F. Nistal, A. Dembinska-Kiec, B. K. W. Beata Kiec-Wilk, A. P. Anna Polus, U. C. Urszula Czech, T. K. Tatiana Konovaleva, G. S. Gerd Schmitz, L. Bertrand, M. Balteau, A. Timmermans, B. Viollet, K. Sakamoto, O. Feron, S. Horman, J. L. Vanoverschelde, C. Beauloye, C. De Meester, E. Martinez, R. Martin, M. Miana, R. Jurado, N. Gomez-Hurtado, M. V. Bartolome, J. A. San Roman, V. Lahera, M. L. Nieto, V. Cachofeiro, F. Rochais, R. Sturny, K. Mesbah, L. Miquerol, R. G. Kelly, S. Messaoudi, B. Gravez, A. Tarjus, V. Pelloux, J. L. Samuel, C. Delcayre, J. M. Launay, K. Clement, N. Farman, F. Jaisser, L. Hadyanto, C. Castellani, G. Vescovo, B. Ravara, R. Tavano, M. Pozzobon, P. De Coppi, E. Papini, R. Vettor, G. Thiene, A. Angelini, M. Meloni, A. Caporali, D. Cesselli, O. Fortunato, E. Avolio, R. Schindler, S. Simrick, T. Brand, N. S. Smart, A. Herman, S. Roura Ferrer, J. Rodriguez Bago, C. Soler-Botija, J. M. Pujal, C. Galvez-Monton, C. Prat-Vidal, A. Llucia-Valldeperas, J. Blanco, A. Bayes-Genis, G. Foldes, M. Maxime, N. N. Ali, M. D. Schneider, S. E. Harding, C. Reni, G. Mangialardi, A. De Pauw, B. Sekkali, A. Friart, H. Ding, A. Graffeuil, D. Catalucci, J. L. Balligand, F. Azibani, F. Tournoux, S. Schlossarek, E. Polidano, L. Fazal, R. Merval, L. Carrier, C. Chatziantoniou, B. Buyandelger, W. Linke, P. Zou, S. Kostin, C. Ku, L. Felkin, E. Birks, P. Barton, M. Sattler, R. Knoell, K. Schroder, S. Benkhoff, H. Shimokawa, O. Grisk, R. P. Brandes, I. R. Parepa, L. Mazilu, A. I. Suceveanu, A. Suceveanu, L. Rusali, L. Cojocaru, L. Matei, M. Toringhibel, E. Craiu, A. L. Pires, M. Pinho, S. Pinho, C. Sena, R. Seica, A. Leite-Moreira, F. Dabroi, S. Schiaffino, E. Kiseleva, N. Krukov, O. Nikitin, L. Ardatova, I. Mourouzis, C. Pantos, A. D. Kokkinos, D. V. Cokkinos, E. Scoditti, M. Massaro, M. A. Carluccio, M. Pellegrino, N. Calabriso, A. Gastaldelli, C. Storelli, R. De Caterina, D. Lindner, C. Zietsch, H.-P. Schultheiss, C. Tschope, D. Westermann, B. R. Everaert, V. J. Nijenhuis, F. C. M. Reith, V. Y. Hoymans, J. P. Timmermans, C. J. Vrints, I. Simova, H. Mateev, T. Katova, L. Haralanov, N. Dimitrov, N. Mironov, S. P. Golitsyn, S. F. Sokolov, Y. U. A. Yuricheva, E. B. Maikov, N. B. Shlevkov, L. V. Rosenstraukh, E. I. Chazov, J. Radosinska, V. Knezl, T. Benova, J. Slezak, L. Urban, N. Tribulova, L. Virag, A. Kristof, Z. S. Kohajda, T. Szel, Z. Husti, I. Baczko, N. Jost, A. Varro, A. Sarusi, A. S. Farkas, S. Z. Orosz, T. Forster, A. Farkas, O. M. Zakhrabova-Zwiauer, M. Hardziyenka, R. Nieuwland, H. L. Tan, A. J. A. Raaijmakers, V. J. A. Bourgonje, G. J. M. Kok, A. A. B. Van Veen, M. E. Anderson, M. A. Vos, M. F. A. Bierhuizen, J. Benes, B. Sebestova, I. A. Ghouri, O. J. Kemi, A. Kelly, F. L. Burton, G. L. Smith, S. Ozdemir, K. Acsai, N. Doisne, R. Van Der Nagel, H. D. M. Beekman, T. A. B. Van Veen, K. R. Sipido, G. Antoons, S. C. Harmer, J. S. Mohal, D. Kemp, A. Tinker, D. Beech, D. S. Burley, C. D. Cox, K. T. Wann, G. F. Baxter, R. Wilders, A. Verkerk, P. Fragkiadaki, G. Germanakis, K. Tsarouchas, C. Tsitsimpikou, M. Tsardi, D. George, A. Tsatsakis, P. Rodrigues, C. Barros, A. K. Najmi, V. Khan, M. Akhtar, K. K. Pillai, M. Mujeeb, M. Aqil, C. R. Bayliss, A. E. Messer, M.-C. Leung, D. Ward, J. Van Der Velden, C. Poggesi, C. S. Redwood, S. Marston, A. Vite, E. Gandjbakhch, F. Gary, V. Fressart, P. Leprince, G. Fontaine, M. Komajda, P. Charron, E. Villard, I. Falcao-Pires, C. Gavina, N. Hamdani, G. J. M. Stienen, H. W. M. Niessens, A. F. Leite-Moreira, W. J. Paulus, M. Memo, S. B. Marston, E. Vafiadaki, J. Qian, D. A. Arvanitis, D. Sanoudou, E. G. Kranias, N. Elmstedt, B. Lind, K. Ferm-Widlund, M. Westgren, L.-A. Brodin, C. Mansfield, T. West, M. Ferenczi, P. J. M. Wijnker, D. B. Foster, A. Coulter, A. Frazier, A. M. Murphy, M. Shah, M. B. Sikkel, T. Desplantez, T. P. Collins, P. O' Gara, A. R. Lyon, K. T. Macleod, A. H. Ottesen, W. E. Louch, C. Carlson, O. J. B. Landsverk, M. Stridsberg, I. Sjaastad, E. Oie, T. Omland, G. Christensen, H. Rosjo, J. Cartledge, L. A. Clark, M. Ibrahim, U. Siedlecka, M. Navaratnarajah, M. H. Yacoub, P. Camelliti, C. M. Terracciano, A. Chester, A. Gonzalez-Tendero, I. Torre, F. Garcia-Garcia, J. Dopazo, E. Gratacos, D. Taylor, S. Bhandari, A.-M. Seymour, D. Fliegner, J. Jost, H. Bugger, R. Ventura-Clapier, A. Carpi, M. Campesan, M. Canton, R. Menabo, P. G. Pelicci, M. Giorgio, F. Di Lisa, M. Hancock, A. Venturini, N. Al-Shanti, C. Stewart, R. Ascione, G. Angelini, M.-S. Suleiman, E. Kravchuk, E. Grineva, M. Galagudza, A. Kostareva, A. Bairamov, K. A. Krychtiuk, L. Watzke, C. Kaun, S. Demyanets, J. Pisoni, S. P. Kastl, K. Huber, G. Maurer, J. Wojta, W. S. Speidl, Z. V. Varga, N. Farago, A. Zvara, G. F. Kocsis, M. Pipicz, C. Csonka, T. Csont, G. L. Puskas, P. Ferdinandy, M. Klevstigova, J. Silhavy, D. Manakov, F. Papousek, J. Novotny, M. Pravenec, F. Kolar, O. Novakova, F. Novak, J. Neckar, J. Barallobre-Barreiro, A. Didangelos, X. Yin, M. Fernandez-Caggiano, I. Drozdov, P. Willeit, N. Domenech, M. Mayr, S. Lemoine, S. Allouche, L. Coulbault, P. Galera, J. L. Gerard, J. L. Hanouz, E. Suveren, M. Whiteman, I. M. Studneva, O. Pisarenko, V. Shulzhenko, L. Serebryakova, O. Tskitishvili, A. Timoshin, J. Fauconnier, A. C. Meli, J. Thireau, S. Roberge, A. M. Lompre, E. Jacotot, A. M. Marks, A. Lacampagne, B. Dietel, R. Altendorf, W. G. Daniel, R. Kollmar, C. D. Garlichs, V. Parente, S. Balasso, G. Pompilio, G. Colombo, G. Milano, L. Squadroni, F. Cotelli, O. Pozzoli, M. C. Capogrossi, Y. Ajiro, N. Saegusa, K. Iwade, W. R. Giles, D. M. Stafforini, K. W. Spitzer, R. Sirohi, L. Candilio, G. Babu, N. Roberts, D. Lawrence, A. Sheikh, S. Kolvekar, J. Yap, D. J. Hausenloy, D. M. Yellon, M. Aslam, S. Rohrbach, K.-D. Schlueter, H. M. Piper, T. Noll, D. Guenduez, L. Malinova, V. P. Ryabukho, D. V. Lyakin, T. P. Denisova, S. Montoro-Garcia, E. Shantsila, G. Y. H. Lip, B. Kalaska, E. Sokolowska, K. Kaminski, K. Szczubialka, K. Kramkowski, A. Mogielnicki, M. Nowakowska, W. Buczko, N. Stancheva, E. Mekenyan, K. Gospodinov, S. Tisheva, A. Darago, I. Rutkai, J. Kalasz, A. Czikora, P. Orosz, H. D. Bjornson, I. Edes, Z. Papp, A. Toth, K. Riches, P. Warburton, D. J. O'regan, S. G. Ball, N. A. Turner, I. C. Wood, K. E. Porter, S. Kogaki, H. Ishida, N. Nawa, K. Takahashi, H. Baden, H. Ichimori, T. Uchikawa, S. Mihara, K. Miura, K. Ozono, R. Lugano, T. Padro, M. Garcia-Arguinzonis, L. Badimon, F. Ferraro, R. Viner, J. Ho, D. Cutler, V. Matchkov, C. Aalkjaer, P. A. J. Krijnen, N. E. Hahn, I. Kholova, J. A. Sipkens, F. P. Van Alphen, S. Simsek, C. G. Schalkwijk, J. D. Van Buul, V. W. M. Van Hinsbergh, H. W. M. Niessen, C. G. Caro, A. Seneviratne, C. Monaco, D. Hou, J. Singh, P. Gilson, M. G. Burke, K. B. Heraty, R. Krams, G. Coppola, K. Albrecht, W. Schgoer, D. Wiedemann, N. Bonaros, C. Steger, M. Theurl, U. Stanzl, R. Kirchmair, S. Amadesi, G. Spinetti, E. Cangiano, M. Valgimigli, A. M. Miller, A. Cardinali, K. Vierlinger, G. Pagano, D. Liccardo, C. Zincarelli, G. D. Femminella, A. Lymperopoulos, C. De Lucia, W. J. Koch, D. Leosco, G. Rengo, R. Hinkel, W. Husada, T. Trenkwalder, Q. Di, S. Lee, B. Petersen, I. Bock-Marquette, H. Niemann, M. Di Maio, C. Kupatt, M. Nourian, Z. Yassin, R. Kelishadi, S. H. Memarian, A. Heidari, A. Leuner, D. M. Poitz, C. Brunssen, U. Ravens, R. H. Strasser, H. Morawietz, F. Vogt, A. Grahl, C. Flege, N. Marx, M. Borinski, B. De Geest, F. Jacobs, I. Muthuramu, S. C. Gordts, E. Van Craeyveld, P. Herijgers, S. Weinert, S. Medunjanin, J. Herold, A. Schmeisser, R. C. Braun-Dullaeus, A. H. Wagner, K. Moeller, O. Adolph, M. Schwarz, C. Schwale, C. Bruehl, R. Nobiling, T. Wieland, S. W. Schneider, M. Hecker, A. Cross, A. Strom, J. Cole, M. Goddard, A. Hultgardh-Nilsson, J. Nilsson, C. Mauri, N. P. Mitkovskaya, T. A. Kurak, E. G. Oganova, E. I. Shkrebneva, Z. H. N. Kot, T. V. Statkevich, F. Molica, F. Burger, C. M. Matter, A. Thomas, C. Staub, A. Zimmer, B. Cravatt, P. Pacher, S. Steffens, R. Blanco, R. Sarmiento, C. Parisi, S. Fandino, F. Blanco, G. Gigena, J. Szarfer, A. Rodriguez, A. Garcia Escudero, M. A. Riccitelli, S. Wantha, S. Simsekyilmaz, R. T. Megens, M. A. Van Zandvoort, E. Liehn, A. Zernecke, D. Klee, C. Weber, O. Soehnlein, L. M. Lima, M. G. Carvalho, K. B. Gomes, I. R. Santos, M. O. Sousa, C. A. S. Morais, S. H. V. Oliveira, I. F. Gomes, F. C. Brandao, M. R. A. Lamego, L. Fornai, A. Kiss, F. Giskes, G. Eijkel, M. Fedrigo, M. L. Valente, R. M. A. Heeren, A. Grdinic, D. Vojvodic, N. Djukanovic, A. G. Grdinic, S. Obradovic, I. Majstorovic, S. Rusovic, Z. Vucinic, D. Tavciovski, M. Ostojic, S.-C. Lai, M.-Y. Chen, H.-T. Wu, L. Gouweleeuw, S. U. Oberdorf-Maass, R. A. De Boer, W. H. Van Gilst, A. H. Maass, I. C. Van Gelder, L. Benard, C. Li, D. Warren, C. M. Shanahan, Q. P. Zhang, A. Bye, R. Vettukattil, S. T. Aspenes, G. Giskeodegaard, I. S. Gribbestad, U. Wisloff, T. F. Bathen, J. Cubedo, R. Alonso, P. Mata, I. Ivic, Z. Vamos, P. Cseplo, D. Kosa, O. Torok, J. Hamar, A. Koller, K. Norita, S. V. De Noronha, M. N. Sheppard, I. Amat-Roldan, I. Iruretagoiena, S. Psilodimitrakopoulos, F. Crispi, D. Artigas, P. Loza-Alvarez, J. C. Harrison, S. D. Smart, E. H. Besely, J. R. Kelly, Y. Yao, I. A. Sammut, M. Hoepfner, W. Kuzyniak, E. Sekhosana, B. Hoffmann, C. Litwinski, A. Pries, E. Ermilov, D. Fontoura, A. P. Lourenco, F. Vasques-Novoa, J. P. Pinto, R. Roncon-Albuquerque, I. P. Oyeyipo, L. A. Olatunji, T. O. Usman, V. A. Olatunji, B. Bacova, C. Viczenczova, V. Dosenko, E. Goncalvesova, J. Vanrooyen, S. K. Maulik, S. Seth, A. K. Dinda, A. Jaiswal, G. Mearini, D. Khajetoorians, E. Kraemer, C. Gedicke-Hornung, G. Precigout, T. Eschenhagen, T. Voit, L. Garcia, S. Lorain, P. Mendes-Ferreira, C. Maia-Rocha, R. Adao, R. J. Cerqueira, M. J. Mendes, P. Castro-Chaves, G. W. De Keulenaer, C. Bras-Silva, G. Ruiter, Y. Y. Wong, M. Lubberink, P. Knaapen, P. Raijmakers, A. A. Lammertsma, J. T. Marcus, N. Westerhof, W. J. Van Der Laarse, A. Vonk-Noordegraaf, N. Steinbronn, E. Koch, G. Steiner, A. Berezin, O. A. Lisovaya, A. M. Soldatova, V. A. Kuznetcov, T. N. Yenina, A. Y. U. Rychkov, P. V. Shebeko, R. Altara, M. H. M. Hessel, J. J. R. Hermans, W. M. Blankesteijn, T. A. Berezina, V. Seden, C. Bonanad, J. Nunez, D. Navarro, M. F. Chilet, F. Sanchis, V. Bodi, G. Minana, F. Chaustre, M. J. Forteza, A. Llacer, G. Galasso, N. Ferrara, A. Akhmedov, R. Klingenberg, C. Brokopp, D. Hof, S. Zoller, R. Corti, S. Gay, A. Von Eckardstein, S. P. Hoerstrup, T. F. Luescher, J. Heijman, A. Zaza, D. M. Johnson, Y. Rudy, R. L. M. Peeters, P. G. A. Volders, R. L. Westra, S. Fujita, R. Okamoto, M. Taniguchi, K. Konishi, I. Goto, K. Sugimoto, M. Nakamura, K. Shiraki, C. Buechler, and M. Ito

Subjects
AMP-activated protein kinase, biology, Physiology, Chemistry, Physiology (medical), Mesenchymal stem cell, biology.protein, Cardiology and Cardiovascular Medicine, Cell biology
Published
2012

4. Saturday, 17 July 2010

Author

I. Dimova, R. Hlushchuk, A. Makanya, V. Djonov, M. Theurl, W. Schgoer, K. Albrecht, A. Beer, J. R. Patsch, P. Schratzberger, S. Mahata, R. Kirchmair, M. Didie, P. Christalla, T. Rau, T. Eschenhagen, U. Schumacher, Q. Lin, M. Zenke, W. Zimmmermann, M. Hoch, P. Fischer, B. Stapel, E. Missol-Kolka, S. Erschow, M. Scherr, H. Drexler, D. Hilfiker-Kleiner, I. Diebold, A. Petry, P. Kennel, T. Djordjevic, J. Hess, A. Goerlach, J. Castellano, R. Aledo, J. Sendra, P. Costales, L. Badimon, V. Llorente-Cortes, E. Dworatzek, S. Mahmoodzadeh, V. Regitz-Zagrosek, A. Posa, C. Varga, A. Berko, M. Veszelka, P. Szablics, B. Vari, I. Pavo, F. Laszlo, M. Brandenburger, J. Wenzel, R. Bogdan, D. Richardt, M. Reppel, J. Hescheler, H. Terlau, A. Dendorfer, J. Heijman, Y. Rudy, R. Westra, P. Volders, R. Rasmusson, V. Bondarenko, M. D. Ertas Gokhan, M. D. Ural Ertan, P. H. D. Karaoz Erdal, P. H. D. Aksoy Ayca, M. D. Kilic Teoman, M. D. Kozdag Guliz, M. D. Vural Ahmet, M. D. Ural Dilek, C. Poulet, T. Christ, E. Wettwer, U. Ravens, C. Van Der Pouw Kraan, S. Schirmer, J. Fledderus, P. Moerland, T. Leyen, J. Piek, N. Van Royen, A. Horrevoets, F. Fleissner, V. Jazbutyte, J. Fiedler, P. Galuppo, M. Mayr, G. Ertl, J. Bauersachs, T. Thum, S. Protze, A. Bussek, F. Li, R. Hoo, K. Lam, A. Xu, P. Subramanian, E. Karshovska, R. Megens, S. Akhtar, K. Heyll, Y. Jansen, C. Weber, A. Schober, M. Zafeiriou, C. Noack, A. Renger, R. Dietz, L. Zelarayan, M. Bergmann, I. Meln, A. Malashicheva, S. Anisimov, N. Kalinina, V. Sysoeva, A. Zaritskey, A. Barbuti, A. Scavone, N. Mazzocchi, A. Crespi, D. Capilupo, D. Difrancesco, L. Qian, W. Shim, Y. Gu, S. Mohammed, P. Wong, M. Zafiriou, H. Schaeffer, P. Kovacs, J. Simon, A. Varro, P. Athias, J. Wolf, O. Bouchot, D. Vandroux, A. Mathe, A. De Carvalho, G. Laurent, P. Rainer, M. Huber, F. Edelmann, T. Stojakovic, A. Trantina-Yates, M. Trauner, B. Pieske, D. Von Lewinski, A. De Jong, A. Maass, S. Oberdorf-Maass, I. Van Gelder, Y. Lin, J. Li, F. Wang, Y. He, X. Li, H. Xu, X. Yang, R. Coppini, C. Ferrantini, C. Ferrara, A. Rossi, A. Mugelli, C. Poggesi, E. Cerbai, N. Rozmaritsa, N. Voigt, D. Dobrev, M.-C. Kienitz, G. Zoidl, K. Bender, L. Pott, Z. Kohajda, A. Kristof, L. Virag, N. Jost, A. Trafford, B. Prnjavorac, E. Mujaric, J. Jukic, K. Abduzaimovic, K. Brack, V. Patel, J. Coote, G. Ng, R. Wilders, A. Van Ginneken, A. Verkerk, P. Xaplanteris, C. Vlachopoulos, K. Baou, C. Vassiliadou, I. Dima, N. Ioakeimidis, C. Stefanadis, W. Ruifrok, C. Qian, H. Sillje, H. Van Goor, D. Van Veldhuisen, W. Van Gilst, R. De Boer, K. Schmidt, F. Kaiser, J. Erdmann, C. De Wit, O. Barnett, Y. Kyyak, F. Cesana, L. Boffi, T. Mauri, M. Alloni, M. Betelli, S. Nava, C. Giannattasio, G. Mancia, R. Vilskersts, J. Kuka, B. Svalbe, E. Liepinsh, M. Dambrova, A. Zakrzewicz, J. Maroski, B. Vorderwuelbecke, K. Fiedorowicz, L. Da Silva-Azevedo, A. Pries, B. Gryglewska, M. Necki, M. Zelawski, T. Grodzicki, E. Scoditti, M. Massaro, M. Carluccio, A. Distante, C. Storelli, R. De Caterina, O. Kocgirli, S. Valcaccia, V. Dao, T. Suvorava, S. Kumpf, M. Floeren, M. Oppermann, G. Kojda, C. Leo, J. Ziogas, J. Favaloro, O. Woodman, W. Goettsch, A. Marton, C. Goettsch, H. Morawietz, E. Khalifa, Z. Ashour, V. Rupprecht, F. Scalera, J. Martens-Lobenhoffer, S. Bode-Boeger, W. Li, Y. Kwan, G. Leung, F. Patella, A. Mercatanti, L. Pitto, G. Rainaldi, I. Tsimafeyeu, Y. Tishova, N. Wynn, S. Kalinchenko, M. Clemente Lorenzo, M. Grande, F. Barriocanal, M. Aparicio, A. Martin, J. Hernandez, J. Lopez Novoa, C. Martin Luengo, A. Kurlianskaya, T. Denisevich, N. Barth, A. Loot, I. Fleming, Y. Wang, A. Gabrielsen, R. Ripa, E. Jorgensen, J. Kastrup, G. Arderiu, E. Pena, K. Kobus, J. Czyszek, A. Kozlowska-Wiechowska, P. Milkiewicz, M. Milkiewicz, R. Madonna, E. Montebello, Y. Geng, J. Chin-Dusting, D. Michell, M. Skilton, J. Dixon, A. Dart, X. Moore, M. Ehrbar, P. Reichmuth, N. Heinimann, B. Hewing, V. Stangl, K. Stangl, M. Laule, G. Baumann, A. Ludwig, R. Widmer-Teske, A. Mueller, P. Stieger, H. Tillmanns, R. Braun-Dullaeus, D. Sedding, K. Troidl, L. Eller, I. Benli, H. Apfelbeck, W. Schierling, C. Troidl, W. Schaper, T. Schmitz-Rixen, R. Hinkel, T. Trenkwalder, A. Pfosser, F. Globisch, G. Stachel, C. Lebherz, I. Bock-Marquette, C. Kupatt, C. Seyler, E. Duthil-Straub, E. Zitron, E. Scholz, D. Thomas, J. Gierten, C. Karle, R. Fink, T. Padro, R. Lugano, M. Garcia-Arguinzonis, M. Schuchardt, J. Pruefer, M. Toelle, N. Pruefer, V. Jankowski, J. Jankowski, W. Zidek, M. Van Der Giet, P. Fransen, C. Van Hove, C. Michiels, J. Van Langen, H. Bult, R. Quarck, M. Wynants, E. Alfaro-Moreno, M. Rosario Sepulveda, F. Wuytack, D. Van Raemdonck, B. Meyns, M. Delcroix, F. Christofi, S. Wijetunge, P. Sever, A. Hughes, J. Ohanian, S. Forman, V. Ohanian, C. Gibbons, S. Vernia, A. Das, V. Shah, M. Casado, W. Bielenberg, J. Daniel, J.-M. Daniel, K. Hersemeyer, T. Schmidt-Woell, D. Kaetzel, H. Tillmans, S. Kanse, E. Tuncay, H. Kandilci, E. Zeydanli, N. Sozmen, D. Akman, S. Yildirim, B. Turan, N. Nagy, K. Acsai, A. Farkas, J. Papp, A. Toth, C. Viero, S. Mason, A. Williams, S. Marston, D. Stuckey, E. Dyer, W. Song, M. El Kadri, G. Hart, M. Hussain, A. Faltinova, J. Gaburjakova, L. Urbanikova, M. Hajduk, B. Tomaskova, M. Antalik, A. Zahradnikova, P. Steinwascher, K. Jaquet, A. Muegge, G. Wang, M. Zhang, C. Tesi, H. Ter Keurs, S. Kettlewell, G. Smith, A. Workman, I. Lenaerts, P. Holemans, S. Sokolow, S. Schurmans, A. Herchuelz, K. Sipido, G. Antoons, X. Wehrens, N. Li, J. R. Respress, A. De Almeida, R. Van Oort, H. Lohmann, M. Saes, A. Messer, O. Copeland, M. Leung, F. Matthes, J. Steinbrecher, G. Salinas-Riester, L. Opitz, G. Hasenfuss, S. Lehnart, G. Caracciolo, M. Eleid, S. Carerj, K. Chandrasekaran, B. Khandheria, P. Sengupta, I. Riaz, L. Tyng, Y. Dou, A. Seymour, C. Dyer, S. Griffin, S. Haswell, J. Greenman, S. Yasushige, P. Amorim, T. Nguyen, M. Schwarzer, F. Mohr, T. Doenst, S. Popin Sanja, D. Lalosevic, I. Capo, T. Momcilov Popin, A. Astvatsatryan, M. Senan, G. Shafieian, N. Goncalves, I. Falcao-Pires, T. Henriques-Coelho, D. Moreira-Goncalves, A. Leite-Moreira, L. Bronze Carvalho, J. Azevedo, M. Andrade, I. Arroja, M. Relvas, G. Morais, M. Seabra, A. Aleixo, J. Winter, M. Zabunova, I. Mintale, D. Lurina, I. Narbute, I. Zakke, A. Erglis, Z. Marcinkevics, S. Kusnere, A. Abolins, J. Aivars, U. Rubins, Y. Nassar, D. Monsef, G. Hamed, S. Abdelshafy, L. Chen, Y. Wu, J. Wang, C. Cheng, M. Sternak, T. Khomich, A. Jakubowski, M. Szafarz, W. Szczepanski, L. Mateuszuk, J. Szymura-Oleksiak, S. Chlopicki, J. Sulicka, M. Strach, I. Kierzkowska, A. Surdacki, T. Mikolajczyk, W. Balwierz, T. Guzik, V. Dmitriev, E. Oschepkova, O. Polovitkina, V. Titov, A. Rogoza, R. Shakur, S. Metcalfe, J. Bradley, S. Demyanets, C. Kaun, S. Kastl, S. Pfaffenberger, I. Huk, G. Maurer, K. Huber, J. Wojta, O. Eriksson, M. Aberg, A. Siegbahn, G. Niccoli, G. Sgueglia, M. Conte, S. Giubilato, N. Cosentino, G. Ferrante, F. Crea, D. Ilisei, M. Leon, F. Mitu, E. Kyriakakis, M. Philippova, M. Cavallari, V. Bochkov, B. Biedermann, G. De Libero, P. Erne, T. Resink, C. Bakogiannis, C. Antoniades, D. Tousoulis, M. Demosthenous, C. Psarros, N. Sfyras, K. Channon, S. Del Turco, T. Navarra, G. Basta, V. Carnicelli, S. Frascarelli, R. Zucchi, A. Kostareva, G. Sjoberg, A. Gudkova, E. Semernin, E. Shlyakhto, T. Sejersen, N. Cucu, M. Anton, D. Stambuli, A. Botezatu, C. Arsene, E. Lupeanu, G. Anton, J. Patsch, E. Huber, C. Lande, A. Cecchettini, L. Tedeschi, M. Trivella, L. Citti, B. Chen, Y. Ma, Y. Yang, X. Ma, F. Liu, M. Hasanzad, L. Rejali, M. Fathi, A. Minassian, R. Mohammad Hassani, A. Najafi, M. Sarzaeem, S. Sezavar, A. Akhmedov, R. Klingenberg, K. Yonekawa, C. Lohmann, S. Gay, W. Maier, M. Neithard, T. Luescher, X. Xie, Z. Fu, A. Kevorkov, L. Verduci, F. Cremisi, A. Wonnerth, K. Katsaros, G. Zorn, T. Weiss, R. De Rosa, G. Galasso, F. Piscione, G. Santulli, G. Iaccarino, R. Piccolo, R. Luciano, M. Chiariello, M. Szymanski, R. Schoemaker, H. Hillege, S. Rizzo, C. Basso, G. Thiene, M. Valente, S. Rickelt, W. Franke, G. Bartoloni, S. Bianca, E. Giurato, C. Barone, G. Ettore, I. Bianca, P. Eftekhari, G. Wallukat, A. Bekel, F. Heinrich, M. Fu, M. Briedert, J. Briand, J. Roegel, K. Pilichou, S. Korkmaz, T. Radovits, S. Pali, K. Hirschberg, S. Zoellner, S. Loganathan, M. Karck, G. Szabo, A. Pucci, J. Pantaleo, S. Martino, G. Pelosi, M. Matteucci, C. Kusmic, N. Vesentini, F. Piccolomini, F. Viglione, A. L'abbate, J. Slavikova, M. Chottova Dvorakova, W. Kummer, A. Campanile, L. Spinelli, M. Ciccarelli, S. De Gennaro, E. Assante Di Panzillo, B. Trimarco, R. Akbarzadeh Najar, S. Ghaderian, A. Tabatabaei Panah, H. Vakili, A. Rezaei Farimani, G. Rezaie, A. Beigi Harchegani, N. Hamdani, C. Gavina, J. Van Der Velden, H. Niessen, G. Stienen, W. Paulus, C. Moura, I. Lamego, C. Eloy, J. Areias, T. Bonda, M. Dziemidowicz, T. Hirnle, I. Dmitruk, K. Kaminski, W. Musial, M. Winnicka, A. Villar, D. Merino, M. Ares, F. Pilar, E. Valdizan, M. Hurle, J. Nistal, V. Vera, P. Karuppasamy, S. Chaubey, T. Dew, R. Sherwood, J. Desai, L. John, M. Marber, G. Kunst, E. Cipolletta, A. Attanasio, C. Del Giudice, P. Campiglia, M. Illario, A. Berezin, E. Koretskaya, E. Bishop, I. Fearon, J. Heger, B. Warga, Y. Abdallah, B. Meyering, K. Schlueter, H. Piper, G. Euler, A. Lavorgna, S. Cecchetti, T. Rio, G. Coluzzi, C. Carrozza, E. Conti, F. Andreotti, A. Glavatskiy, O. Uz, E. Kardesoglu, O. Yiginer, S. Bas, O. Ipcioglu, N. Ozmen, M. Aparci, B. Cingozbay, F. Ivanes, M. Hillaert, S. Susen, F. Mouquet, P. Doevendans, B. Jude, G. Montalescot, E. Van Belle, C. Castellani, A. Angelini, O. De Boer, C. Van Der Loos, G. Gerosa, A. Van Der Wal, I. Dumitriu, P. Baruah, J. Kaski, O. Maytham, J. D Smith, M. Rose, A. Cappelletti, A. Pessina, M. Mazzavillani, G. Calori, A. Margonato, S. Cassese, C. D'anna, A. Leo, A. Silenzi, M. Baca', L. Biasucci, D. Baller, U. Gleichmann, J. Holzinger, T. Bitter, D. Horstkotte, A. Antonopoulos, A. Miliou, C. Triantafyllou, W. Masson, D. Siniawski, P. Sorroche, L. Casanas, W. Scordo, J. Krauss, A. Cagide, T. Huang, A. Wiedon, S. Lee, K. Walker, K. O'dea, P. Perez Berbel, V. Arrarte Esteban, M. Garcia Valentin, M. Sola Villalpando, C. Lopez Vaquero, L. Caballero, M. Quintanilla Tello, F. Sogorb Garri, G. Duerr, N. Elhafi, T. Bostani, L. Swieny, E. Kolobara, A. Welz, W. Roell, O. Dewald, N. Kaludercic, E. Takimoto, T. Nagayama, K. Chen, J. Shih, D. Kass, F. Di Lisa, N. Paolocci, L. Vinet, M. Pezet, F. Briec, M. Previlon, P. Rouet-Benzineb, A. Hivonnait, F. Charpentier, J. Mercadier, M. Cobo, M. Llano, C. Montalvo, V. Exposito, L. Meems, B. Westenbrink, L. Biesmans, V. Bito, R. Driessen, C. Huysmans, I. Mourouzis, C. Pantos, G. Galanopoulos, M. Gavra, P. Perimenis, D. Spanou, D. Cokkinos, T. Panasenko, S. Partsch, C. Harjung, A. Bogdanova, D. Mihov, P. Mocharla, S. Yakushev, J. Vogel, M. Gassmann, R. Tavakoli, D. Johansen, E. Sanden, C. Xi, R. Sundset, K. Ytrehus, M. Bliksoen, A. Rutkovskiy, L. Mariero, I. Vaage, K. Stenslokken, O. Pisarenko, V. Shulzhenko, I. Studneva, L. Serebryakova, O. Tskitishvili, Y. Pelogeykina, A. Timoshin, A. Vanin, L. Ziberna, M. Lunder, G. Drevensek, S. Passamonti, L. Gorza, B. Ravara, C. Scapin, M. Vitadello, F. Zigrino, J. Gwathmey, F. Del Monte, G. Vilahur, O. Juan-Babot, B. Onate, L. Casani, S. Lemoine, G. Calmettes, B. Jaspard-Vinassa, C. Duplaa, T. Couffinhal, P. Diolez, P. Dos Santos, A. Fusco, D. Sorriento, P. Cervero, A. Feliciello, E. Barnucz, K. Kozichova, M. Hlavackova, J. Neckar, F. Kolar, O. Novakova, F. Novak, C. Barsanti, N. Abraham, D. Muntean, S. Mirica, O. Duicu, A. Raducan, M. Hancu, O. Fira-Mladinescu, V. Ordodi, J. Voelkl, B. Haubner, G. Neely, C. Moriell, S. Seidl, O. Pachinger, J. Penninger, and B. Metzler

Subjects
Physiology, Physiology (medical), Cardiology and Cardiovascular Medicine
Published
2010

8. D-glucose uptake in isolated cells of lobster hepatopancreatic epithelium

Author

VERRI T, L. ZILLI, A. MANDAL, D. BOSSA, P. K. MANDAL, L. INGROSSO, V. ZONNO, G. AHEARN, C. STORELLI, VILELLA, Sebastiano, Verri, T, Zilli, L, Mandal, A, Bossa, D, Mandal, Pk, Ingrosso, L, Zonno, V, Vilella, Sebastiano, Ahearn, Ga, Storelli, C., L., Zilli, A., Mandal, D., Bossa, P. K., Mandal, L., Ingrosso, V., Zonno, G., Ahearn, and C., Storelli

Published
2000

10. Original article: Steroid receptor status in malignant and non-malignant larynx

Author

S. Marsigliante, G. Leo, Leonardo Resta, and C. Storelli

Subjects
medicine.medical_specialty, medicine.drug_class, business.industry, Hematology, medicine.disease, Androgen, Metastasis, Endocrinology, medicine.anatomical_structure, Oncology, Estrogen, Internal medicine, medicine, Carcinoma, Receptor, business, Lymph node, Glucocorticoid, medicine.drug, Hormone
Abstract

Summary We investigated for the first time the relationships among all the different steroid receptor classes and between steroid receptor status and lymph node involvement in laryn-geal carcinoma. Androgen (AR), oestrogen (ER), progesterone (PR) and glucocorticoid (GR) receptors were assayed in the high-speed soluble fraction and in the nuclear extract from 73 carcinomas of the larynx. Forty-one, 26, 15, and 13 tumours expressed cytosolic GR, ER, AR, and PR, respectively, while 33, 26, 13 and 13 biopsies were nuclear-positive for GR, ER, AR, and PR, respectively. Data obtained in histologically-proven non-cancerous larynx (N = 20) compared to those obtained in the malignant specimens showed a significant loss of ER and PR in cancerous larynx over that in the non-cancerous tissue. Lymph node metastases were evaluated in only 53 of the 73 patients and they were noted in 22 cases (41.5%). No significant relationships were found either among the different classes of steroid receptors or between steroid receptors and lymph node involvement. Despite the apparent absence of any interrelationships among the different receptors or tendency towards metastasis, the presence of steroid receptors would justify the use of hormonal manipulations which could be effective in the management of this disease.

Published
1992

11. Optical characterization of glutamate dehydrogenase monolayers chemisorbed on SiO2

Author

P P, Pompa, L, Blasi, L, Longo, R, Cingolani, G, Ciccarella, G, Vasapollo, R, Rinaldi, A, Rizzello, C, Storelli, and M, Maffia

Subjects
Silicon, Time Factors, Light, Propylamines, Protein Conformation, Biophysics, Temperature, Tryptophan, Silanes, Silicon Dioxide, Biophysical Phenomena, Spectrometry, Fluorescence, Glutamate Dehydrogenase, Spectroscopy, Fourier Transform Infrared, Scattering, Radiation
Abstract

This paper describes the formation of glutamate dehydrogenase monolayers on silicon dioxide, and their characterization by means of physical techniques, i.e., fluorescence spectroscopy and Fourier-transform infrared spectroscopy. Detailed investigations of the intrinsic stability of native proteins in solution were carried out to elucidate the occurrence of conformational changes induced by the immobilization procedure. The enzyme monolayers were deposited on SiO2 after preexposing silicon surfaces to 3-aminopropyltriethoxysilane and reacting the silylated surfaces with glutaric dialdehyde. The optical characterization demonstrates that the immobilization does not interfere with the fold pattern of the native enzyme. In addition, fluorescence spectroscopy, thermal denaturation, and quenching studies performed on the enzyme in solution well describe the folding and unfolding properties of glutamate dehydrogenase. The photophysical studies reported here are relevant for nanobioelectronics applications requiring protein immobilization on a chip.

Published
2002

14. Steroid receptor status in malignant and non-malignant larynx

Author

S, Marsigliante, G, Leo, L, Resta, and C, Storelli

Subjects
Adult, Cell Nucleus, Male, Aging, Receptors, Steroid, Middle Aged, Immunoenzyme Techniques, Cytosol, Receptors, Glucocorticoid, Receptors, Estrogen, Receptors, Androgen, Lymphatic Metastasis, Humans, Larynx, Receptors, Progesterone, Laryngeal Neoplasms, Aged
Abstract

We investigated for the first time the relationships among all the different steroid receptor classes and between steroid receptor status and lymph node involvement in laryngeal carcinoma. Androgen (AR), oestrogen (ER), progesterone (PR) and glucocorticoid (GR) receptors were assayed in the high-speed soluble fraction and in the nuclear extract from 73 carcinomas of the larynx. Forty-one, 26, 15, and 13 tumours expressed cytosolic GR, ER, AR, and PR, respectively, while 33, 26, 13 and 13 biopsies were nuclear-positive for GR, ER, AR, and PR, respectively. Data obtained in histologically-proven non-cancerous larynx (N = 20) compared to those obtained in the malignant specimens showed a significant loss of ER and PR in cancerous larynx over that in the non-cancerous tissue. Lymph node metastases were evaluated in only 53 of the 73 patients and they were noted in 22 cases (41.5%). No significant relationships were found either among the different classes of steroid receptors or between steroid receptors and lymph node involvement. Despite the apparent absence of any interrelationships among the different receptors or tendency towards metastasis, the presence of steroid receptors would justify the use of hormonal manipulations which could be effective in the management of this disease.

Published
1992

16. Mitogenic signalling by B2 bradykinin receptor in epithelial breast cells.

Author

S. Greco, A. Muscella, M.G. Elia, S. Romano, C. Storelli, and Santo Marsigliante

Subjects
EPITHELIAL cells, BREAST, BRADYKININ, MITOGENS
Abstract

The kinin peptides are released during inflammation and are amongst the most potent known mediators of vasodilatation, pain, and oedema. A role in the modulation or induction of healthy breast tissue growth has been postulated for tissue kallikrein present in human milk. Moreover, tissue kallikrein was found in malignant human breast tissue and bradykinin (BK) stimulates the proliferation of immortalised breast cancer cells. Aim of the present article was to investigate whether BK also exerts mitogenic activity in normal breast epithelial cells and partially characterise the signalling machinery involved. Results show that BK increased up to 2‐fold the 24 h proliferation of breast epithelial cells in primary culture, and that the BK B2 receptor (not B1) inhibitor alone fully blocked the BK response. Intracellular effects of B2 stimulation were the following: (a) the increase of free intracellular Ca2+ concentration by a mechanism dependent upon the phospholipase C (PLC) activity; (b) the cytosol‐to‐membrane translocation of conventional (PKC)‐α and ‐β isozymes, novel PKC‐δ, ‐ɛ, and ‐η isozymes; (c) the phosphorylation of the extracellular‐regulated kinase 1 and 2 (ERK1/2); and (d) the stimulation of the expression of c‐Fos protein. EGF, a well known stimulator of cell proliferation, regulated the proliferative response in human epithelial breast cells to the same extent of BK. The effects of BK on proliferation, ERK1/2 phosphorylation, and c‐Fos expression were abolished by GF109203X, which inhibits PKC‐δ isozyme. Conversely, Gö6976, an inhibitor of PKC‐α and ‐β isozymes, and the 18‐h treatment of cells with PMA, that led to the complete down‐regulation of PKC‐α, ‐β, ‐ɛ, and ‐η, but not of PKC‐δ, did not have any effect, thereby indicating that the PKC‐δ mediates the mitogenic signalling of BK. Phosphoinositide 3‐kinase (PI3K), tyrosine kinase of the epidermal growth factor receptor (EGFR), and mitogen activated protein kinase kinases (MEK) inhibitors were also tested. The results suggest that EGFR, PI3K, and ERK are required for the proliferative effects of BK. In addition, the BK induced cytosol‐to‐membrane translocation of PKC‐δ was blocked by PI3K inhibition, suggesting that PI3K is upstream to PKC‐δ. In conclusion, BK has mitogenic actions in cultured human epithelial breast cells; the activation of PKC‐δ through B2 receptor acts in concert with ERK and PI3K pathways to induce cell proliferation. J. Cell. Physiol. 201: 84–96, 2004. © 2004 Wiley‐Liss, Inc. [ABSTRACT FROM AUTHOR]

Published
2004
Full Text
View/download PDF

17. Angiotensin II activates extracellular signal regulated kinases via protein kinase C and epidermal growth factor receptor in breast cancer cells.

Author

S. Greco, A. Muscella, M.G. Elia, P. Salvatore, C. Storelli, A. Mazzotta, C. Manca, and S. Marsigliante

Subjects
ANGIOTENSINS, ANGIOTENSIN II, BREAST, BREAST cancer
Abstract

Angiotensin II (Ang II) induces, through AT1, intracellular Ca2+ increase in both normal and cancerous breast cells in primary culture (Greco et al., 2002 Cell Calcium 2:1–10). We here show that Ang II stimulated, in a dose-dependent manner, the 24 h-proliferation of breast cancer cells in primary culture, induced translocation of protein kinase C (PKC)-α, -β1/2, and δ (but not -ε, -η, -θ, -ζ, and -ι), and phosphorylated extracellular-regulated kinases 1 and 2 (ERK1/2). The proliferative effects of Ang II were blocked by the AT1 antagonist, losartan. Also epidermal growth factor (EGF) had mitogenic effects on serum-starved breast cancer cells since induced cell proliferation after 24 h and phosphorylation of ERK1/2. The Ang II-induced proliferation of breast cancer cells was reduced by (a) Gö6976, an inhibitor of conventional PKC-α and -β1, (b) AG1478, an inhibitor of the tyrosine kinase of the EGF receptor (EGFR), and (c) downregulation of 1,2-diacylglycerol-sensitive PKCs achieved by phorbol 12-myristate 13-acetate (PMA). A complete inhibition of the Ang II-induced cell proliferation was achieved using the inhibitor of the mitogen activated protein kinase kinase (MAPKK or MEK), PD098059, or using Gö6976 together with AG1478. These results indicate that in human primary cultured breast cancer cells AT1 regulates mitogenic signaling pathways by two simultaneous mechanisms, one involving conventional PKCs and the other EGFR transactivation. J. Cell. Physiol. 196: 370–377, 2003. © 2003 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Published
2003
Full Text
View/download PDF

19. [Uptake of L-(+)lactate by cell membrane (luminal and contraluminal) isolated from rat small intestine microvilli]

Author

A, Corcelli, C, Storelli-Joss, C, Lippe, and C, Storelli

Subjects
Monocarboxylic Acid Transporters, Microvilli, Cell Membrane, Osmolar Concentration, Biological Transport, Sodium Chloride, Potassium Chloride, Rats, Cinnamates, Intestine, Small, Nitriles, Centrifugation, Density Gradient, Lactates, Animals, Pyruvates
Abstract

L-lactate uptake was measured in vesicles formed by intestinal brush border and baso-lateral membranes, using a rapid filtration technique. In the presence of a Na+ gradient directed into the vesicle, L-lactate can be transiently accumulated in brush border vesicles, but not in baso-lateral ones. The transient L-lactate accumulation does not occur in the presence of a KCl gradient. alpha-cyanocinammic acid strongly inhibits L-lactate uptake in brush border vesicles, but not in baso-lateral ones. These results support the existence of a carrier mediated, Na+ dependent, transport of L-lactate across the brush border membrane.

Published
1979

24. [Glycine uptake in brush border vesicles isolated from the rat intestinal cells]

Author

A, Corcelli, G, Rago, V, Scalera, and C, Storelli

Subjects
Intestines, Microvilli, Osmolar Concentration, Glycine, Animals, Biological Transport, Active, Sodium Chloride, Rats
Abstract

The uptake of glycine in osmotically active brush border membrane vesicles (obtained by the Mg++ precipitation method) has been studied and a partial characterization of its transport system has been established. The glycine uptake in these vesicles was stimulated by the presence of sodium and in the presence of an inwardly directed Na+ -gradient glycine was accumulated inside the vesicles. The effect of Na+ was specific; other monovalent cation as Li+, K+, Rb+ and choline were uneffective in the stimulation of glycine uptake, under the same experimental conditions. Preliminary experiments show an important role of some anions on the glycine uptake. A strong inhibition in the uptake rate was found when the measurements were carried out in the presence of sodium cyclamate, while in the presence of NaSCN the measured uptake values were similar to those observed in the presence of NaCl.

Published
1983

27. [A disaccharidase associated glucose transport system]

Author

H, Vögeli, C, Storelli, and G, Semenza

Subjects
Cell Membrane Permeability, Glucose, Glycoside Hydrolases, Intestinal Absorption, Intestine, Small, Animals, Biological Transport, Fructose, Rabbits, Chromatography, Ion Exchange
Published
1972

32. miR-155 is up-regulated in primary and secondary glioblastoma and promotes tumour growth by inhibiting GABA receptors

Author

Massimo Mallardo, Oscar Fernando D'Urso, Cosimo Damiano Gianfreda, Caliandro Pietro, Antonio Montinaro, Santo Marsigliante, Antonia Cimmino, Carlo Storelli, Pietro I. D'Urso, Pi, D'Urso, Of, D'Urso, C., Storelli, Mallardo, Massimo, Cd, Gianfreda, A., Montinaro, A., Cimmino, C., Pietro, S. M. a. r. s. i. g. l. i. a. n. t., E., D'Urso, Pi, D'Urso, Of, Storelli, Carlo, Mallardo, M, Gianfreda, Cd, Montinaro, A, Cimmino, A, Pietro, C, and Marsigliante, Santo

Subjects
Adult, Male, Cancer Research, Survival, Cell, Biology, Real-Time Polymerase Chain Reaction, survival, Diagnosis, Differential, miR-155, Young Adult, Gene expression, microRNA, Tumor Cells, Cultured, medicine, Cluster Analysis, Humans, Gene silencing, Microarray, Aged, Oligonucleotide Array Sequence Analysis, Oncogene, Brain Neoplasms, Cell growth, Gene Expression Profiling, glioblastoma, MicroRNA, Middle Aged, Cell cycle, Receptors, GABA-A, Up-Regulation, Gene Expression Regulation, Neoplastic, MicroRNAs, Cell Transformation, Neoplastic, medicine.anatomical_structure, Oncology, gene expression, Cancer research, Female, Glioblastoma, microarray
Abstract

An altered expression of microRNAs (miRNAs) contributes both to the development of cancer and to the progression of the disease. Malignant tumours and tumour cell lines have widespread deregulated expressions of miRNAs compared to normal tissues. In this study, we investigated the expression profiles of 340 mammalian miRNAs in 93 cases of multiform glioblastoma (primary and secondary glioblastoma tumours), by means of DNA microarrays. We show that the expression profiles of 10 miRNAs can distinguish primary from secondary glioblastoma types. Moreover, we found elevated miR-155 levels in primary and secondary glioblastoma tissues as well as in glioblastoma primary cultures. We hypoth- esised that γ-aminobutyric acid A receptor 1 (GABRA1) is a miR-155 target, and studied the correlation between miR-155 up-regulation and the GABRA1 protein in cultured glioblas- toma cells by miRNA silencing. We show that a decrease in miR-155 expression to normal levels restores the expression of GABRA1, making glioblastoma cells sensitive to signals that inhibit cell proliferation mediated by GABRA1. In conclu- sion, the expression patterns of different miRNAs characterise primary and secondary glioblastomas. The aberrant overex- pression of miR-155 contributes to the malignant phenotype of glioblastoma cells removing growth inhibition. * Contributed equally

Published
2012

33. D-Glucose transport in decapod crustacean hepatopancreas

Author

P.K. Mandal, Loredana Zilli, G. A. Ahearn, D Bossa, Sebastiano Vilella, V. Zonno, Tiziano Verri, L. Ingrosso, Carlo Storelli, A. Mandal, Verri, Tiziano, A., Mandal, L., Zilli, D., Bossa, P. K., Mandal, L., Ingrosso, V., Zonno, Vilella, Sebastiano, G. A., Ahearn, Storelli, Carlo, Verri, T, G., Ahearn, and C., Storelli

Subjects
medicine.medical_specialty, Homarus americanu, Physiology, Xenopus, Carbohydrate metabolism, Penaeus japonicu, Biochemistry, Absorption, Internal medicine, Crustacea, expression, medicine, Animals, Molecular Biology, Gastrointestinal tract, biology, hepatopancrea, Midgut, Biological Transport, Metabolism, biology.organism_classification, Crustacean, Endocrinology, Glucose, uptake, D-glucose transport, Hepatopancreas, Xenopus laevis oocytes, Digestive System, Hormone
Abstract

Physiological mechanisms of gastrointestinal absorption of organic solutes among crustaceans remain severely underinvestigated, in spite of the considerable relevance of characterizing the routes of nutrient absorption for both nutritional purposes and formulation of balanced diets in aquaculture. Several lines of evidence attribute a primary absorptive role to the digestive gland (hepatopancreas) and a secondary role to the midgut (intestine). Among absorbed organic solutes, the importance of D-glucose in crustacean metabolism is paramount. Its plasma levels are finely tuned by hormones (crustacean hyperglycemic hormone, insulin-like peptides and insulin-like growth factors) and the function of certain organs (i.e. brain and muscle) largely depends on a balanced D-glucose supply. In the last few decades, D-glucose absorptive processes of the gastrointestinal tract of crustaceans have been described and transport mechanisms investigated, but not fully disclosed. We briefly review our present knowledge of D-glucose transport processes in the crustacean hepatopancreas. A discussion of previous results from experiments with hepatopancreatic epithelial brush-border membrane vesicles is presented. In addition, recent advances in our understandings of hepatopancreatic D-glucose transport are shown, as obtained (1) after isolation of purified R-, F-, B- and E-cell suspensions from the whole organ by centrifugal elutriation, and (2) by protein expression in hepatopancreatic mRNA-injected Xenopus laevis oocytes. In a perspective, the applicability of these novel methods to the study of hepatopancreatic absorptive function will certainly improve our knowledge of this structurally complex organ.

Published
2001

34. Carnosine modulates the Sp1-Slc31a1/Ctr1 copper-sensing system and influences copper homeostasis in murine CNS-derived cells.

Author

Barca A, Ippati S, Urso E, Vetrugno C, Storelli C, Maffia M, Romano A, and Verri T

Subjects
Animals, Brain cytology, Brain drug effects, Cells, Cultured, Copper Transporter 1, Dose-Response Relationship, Drug, Homeostasis drug effects, Homeostasis physiology, Male, Mice, Mice, Inbred BALB C, Brain metabolism, Carnosine pharmacology, Cation Transport Proteins metabolism, Copper metabolism, Sp1 Transcription Factor metabolism
Abstract

Carnosine (CAR) is an endogenous dipeptide physiologically present in excitable tissues, such as central nervous system (CNS) and muscle. CAR is acknowledged as a substrate involved in many homeostatic pathways and mechanisms and, due to its biochemical properties, as a molecule intertwined with the homeostasis of heavy metals such as copper (Cu). In CNS, Cu excess and dysregulation imply oxidative stress, free-radical production, and functional impairment leading to neurodegeneration. Here, we report that CAR intercepts the regulatory routes of Cu homeostasis in nervous cells and tissues. Specifically, in a murine neuron-derived cell model, i.e., the B104 neuroblastoma cells, extracellular CAR exposure up to 24 h influenced intracellular Cu entry and affected (downregulated) the key Cu-sensing system, consisting of the gene coding for the Slc31a1 transmembrane Cu importer (alias Ctr1), and the gene coding for the Cu-responsive transcription factor Sp1 ( Sp1). Also, CAR exposure upregulated CAR biosynthesis ( Carns1), extracellular degradation ( Cndp1), and transport ( Slc15a4, alias Pht1) genes and elicited CAR intracellular accumulation, contributing to the outline of functional association between CAR and Cu within the cell. Interestingly, the same gene modulation scheme acting in vitro operates in vivo in brains of mice undergoing dietary administration of CAR in drinking water for 2 wk. Overall, our findings describe for the first time a regulatory interaction between CAR and Cu pathways in CNS and indicate CAR as a novel active molecule within the network of ligands and chaperones that physiologically regulate Cu homeostasis.

Published
2019
Full Text
View/download PDF

35. Di- and tripeptide transport in vertebrates: the contribution of teleost fish models.

Author

Verri T, Barca A, Pisani P, Piccinni B, Storelli C, and Romano A

Subjects
Animals, Humans, Models, Animal, Fish Proteins metabolism, Fishes metabolism, Oligopeptides metabolism, Symporters metabolism
Abstract

Solute Carrier 15 (SLC15) family, alias H + -coupled oligopeptide cotransporter family, is a group of membrane transporters known for their role in the cellular uptake of di- and tripeptides (di/tripeptides) and peptide-like molecules. Of its members, SLC15A1 (PEPT1) chiefly mediates intestinal absorption of luminal di/tripeptides from dietary protein digestion, while SLC15A2 (PEPT2) mainly allows renal tubular reabsorption of di/tripeptides from ultrafiltration, SLC15A3 (PHT2) and SLC15A4 (PHT1) possibly interact with di/tripeptides and histidine in certain immune cells, and SLC15A5 has unknown function. Our understanding of this family in vertebrates has steadily increased, also due to the surge of genomic-to-functional information from 'non-conventional' animal models, livestock, poultry, and aquaculture fish species. Here, we review the literature on the SLC15 transporters in teleost fish with emphasis on SLC15A1 (PEPT1), one of the solute carriers better studied amongst teleost fish because of its relevance in animal nutrition. We report on the operativity of the transporter, the molecular diversity, and multiplicity of structural-functional solutions of the teleost fish orthologs with respect to higher vertebrates, its relevance at the intersection of the alimentary and osmoregulative functions of the gut, its response under various physiological states and dietary solicitations, and its possible involvement in examples of total body plasticity, such as growth and compensatory growth. By a comparative approach, we also review the few studies in teleost fish on SLC15A2 (PEPT2), SLC15A4 (PHT1), and SLC15A3 (PHT2). By representing the contribution of teleost fish to the knowledge of the physiology of di/tripeptide transport and transporters, we aim to fill the gap between higher and lower vertebrates.

Published
2017
Full Text
View/download PDF

36. Therapeutic potential of the dual peroxisome proliferator activated receptor (PPAR)α/γ agonist aleglitazar in attenuating TNF-α-mediated inflammation and insulin resistance in human adipocytes.

Author

Massaro M, Scoditti E, Pellegrino M, Carluccio MA, Calabriso N, Wabitsch M, Storelli C, Wright M, and De Caterina R

Subjects
Adipocytes metabolism, Adipocytes physiology, Adiponectin genetics, Cell Line, Cell Movement drug effects, Cell Survival drug effects, Chemokine CCL2 genetics, Chemokine CXCL10 genetics, Gene Expression Regulation drug effects, Glucose metabolism, Humans, Inflammation genetics, Inflammation metabolism, Insulin Resistance, Interleukin-6 genetics, Lipid Metabolism drug effects, p38 Mitogen-Activated Protein Kinases metabolism, Adipocytes drug effects, Hypoglycemic Agents pharmacology, Oxazoles pharmacology, PPAR alpha agonists, PPAR gamma agonists, Thiophenes pharmacology, Tumor Necrosis Factor-alpha pharmacology
Abstract

Adipose tissue inflammation is a mechanistic link between obesity and its related sequelae, including insulin resistance and type 2 diabetes. Dual ligands of peroxisome proliferator activated receptor (PPAR)α and γ, combining in a single molecule the metabolic and inflammatory-regulatory properties of α and γ agonists, have been proposed as a promising therapeutic strategy to antagonize adipose tissue inflammation. Here we investigated the effects of the dual PPARα/γ agonist aleglitazar on human adipocytes challenged with inflammatory stimuli. Human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes were treated with aleglitazar or - for comparison - the selective agonists for PPARα or γ fenofibrate or rosiglitazone, respectively, for 24h before stimulation with TNF-α. Aleglitazar, at concentrations as low as 10nmol/L, providing the half-maximal transcriptional activation of both PPARα and PPARγ, reduced the stimulated expression of several pro-inflammatory mediators including interleukin (IL)-6, the chemokine CXC-L10, and monocyte chemoattractant protein (MCP)-1. Correspondingly, media from adipocytes treated with aleglitazar reduced monocyte migration, consistent with suppression of MCP-1 secretion. Under the same conditions, aleglitazar also reversed the TNF-α-mediated suppression of insulin-stimulated ser473 Akt phosphorylation and decreased the TNF-α-induced ser312 IRS1 phosphorylation, two major switches in insulin-mediated metabolic activities, restoring glucose uptake in insulin-resistant adipocytes. Such effects were similar to those obtainable with a combination of single PPARα and γ agonists. In conclusion, aleglitazar reduces inflammatory activation and dysfunction in insulin signaling in activated adipocytes, properties that may benefit diabetic and obese patients. The effect of aleglitazar was consistent with dual PPARα and γ agonism, but with no evidence of synergism., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Published
2016
Full Text
View/download PDF

38. Multiple anti-inflammatory and anti-atherosclerotic properties of red wine polyphenolic extracts: differential role of hydroxycinnamic acids, flavonols and stilbenes on endothelial inflammatory gene expression.

Author

Calabriso N, Scoditti E, Massaro M, Pellegrino M, Storelli C, Ingrosso I, Giovinazzo G, and Carluccio MA

Subjects
Anti-Inflammatory Agents analysis, Atherosclerosis drug therapy, Cell Adhesion drug effects, Chemokine CCL2 genetics, Chemokine CCL2 metabolism, Coumaric Acids analysis, E-Selectin genetics, E-Selectin metabolism, Endothelial Cells drug effects, Flavonols analysis, Humans, Inflammation drug therapy, Intercellular Adhesion Molecule-1 genetics, Intercellular Adhesion Molecule-1 metabolism, Italy, NF-kappa B genetics, NF-kappa B metabolism, Oxidative Stress drug effects, Polyphenols analysis, RNA, Messenger genetics, RNA, Messenger metabolism, Stilbenes analysis, Transcription Factor AP-1 genetics, Transcription Factor AP-1 metabolism, Vascular Cell Adhesion Molecule-1 genetics, Vascular Cell Adhesion Molecule-1 metabolism, Anti-Inflammatory Agents pharmacology, Coumaric Acids pharmacology, Flavonols pharmacology, Polyphenols pharmacology, Stilbenes pharmacology, Wine analysis
Abstract

Purpose: The aim of the study was to evaluate the vascular anti-inflammatory effects of polyphenolic extracts from two typical South Italy red wines, the specific contribution of individual polyphenols and the underlying mechanisms of action., Methods: Human endothelial cells were incubated with increasing concentrations (1-50 μg/mL) of Primitivo and Negroamaro polyphenolic extracts (PWPE and NWPE, respectively) or pure polyphenols (1-25 μmol/L), including hydroxycinnamic acids (p-coumaric, caffeic and caftaric acids), flavonols (kaempferol, quercetin, myricetin) or stilbenes (trans-resveratrol, trans-piceid) before stimulation with lipopolysaccharide. Through multiple assays, we analyzed the endothelial-monocyte adhesion, the endothelial expression of adhesion molecules (ICAM-1, VCAM-1 and E-Selectin), monocyte chemoattractant protein-1 (MCP-1) and macrophage colony-stimulating factor (M-CSF), as well as ROS intracellular levels and the activation of NF-κB and AP-1., Results: Both PWPE and NWPE, already at 1 μg/mL, inhibited monocyte adhesion to stimulated endothelial cells, a key event in triggering vascular inflammation. They down-regulated the expression of adhesion molecules, ICAM-1, VCAM-1, E-Selectin, as well as MCP-1 and M-CSF, at mRNA and protein levels. All polyphenols reduced intracellular ROS, and everything, except caftaric acid, inhibited the endothelial expression of adhesion molecules and MCP-1, although with different potency. Flavonols and resveratrol significantly reduced also the endothelial expression and release of M-CSF. The decrease in endothelial inflammatory gene expression was related to the inhibition of NF-κB and AP-1 activation but not to intracellular oxidative stress., Conclusions: This study showed multiple anti-inflammatory and anti-atherosclerotic properties of red wine polyphenolic extracts and indentified specific bioactive polyphenols which could counteract inflammatory diseases including atherosclerosis.

Published
2016
Full Text
View/download PDF

39. Extra virgin olive oil rich in polyphenols modulates VEGF-induced angiogenic responses by preventing NADPH oxidase activity and expression.

Author

Calabriso N, Massaro M, Scoditti E, D'Amore S, Gnoni A, Pellegrino M, Storelli C, De Caterina R, Palasciano G, and Carluccio MA

Subjects
Endothelium, Vascular cytology, Endothelium, Vascular drug effects, Endothelium, Vascular enzymology, Human Umbilical Vein Endothelial Cells, Humans, NADPH Oxidases antagonists & inhibitors, Neovascularization, Pathologic prevention & control, Olive Oil chemistry, Polyphenols pharmacology, Vascular Endothelial Growth Factor A physiology
Abstract

Previous studies have shown the antiinflammatory, antioxidant and antiangiogenic properties by pure olive oil polyphenols; however, the effects of olive oil phenolic fraction on the inflammatory angiogenesis are unknown. In this study, we investigated the effects of the phenolic fraction (olive oil polyphenolic extract, OOPE) from extra virgin olive oil and related circulating metabolites on the VEGF-induced angiogenic responses and NADPH oxidase activity and expression in human cultured endothelial cells. We found that OOPE (1-10 μg/ml), at concentrations achievable nutritionally, significantly reduced, in a concentration-dependent manner, the VEGF-induced cell migration, invasiveness and tube-like structure formation through the inhibition of MMP-2 and MMP-9. OOPE significantly (P<0.05) reduced VEGF-induced intracellular reactive oxygen species by modulating NADPH oxidase activity, p47phox membrane translocation and the expression of Nox2 and Nox4. Moreover, the treatment of endothelial cells with serum obtained 4 h after acute intake of extra virgin olive oil, with high polyphenol content, decreased VEGF-induced NADPH oxidase activity and Nox4 expression, as well as, MMP-9 expression, as compared with fasting control serum. Overall, native polyphenols and serum metabolites of extra virgin olive oil rich in polyphenols are able to lower the VEGF-induced angiogenic responses by preventing endothelial NADPH oxidase activity and decreasing the expression of selective NADPH oxidase subunits. Our results provide an alternative mechanism by which the consumption of olive oil rich in polyphenols may account for a reduction of oxidative stress inflammatory-related sequelae associated with chronic degenerative diseases., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Published
2016
Full Text
View/download PDF

40. miR-15b and miR-21 as Circulating Biomarkers for Diagnosis of Glioma.

Author

Ivo D'Urso P, Fernando D'Urso O, Damiano Gianfreda C, Mezzolla V, Storelli C, and Marsigliante S

Abstract

Malignant gliomas are lethal primary intracranial tumors. To date, little information on the role of deregulated genes in gliomas have been identified. As the involvement of miRNAs in the carcinogenesis is well known, we carried out a pilot study to identify, as potential biomarkers, differentially expressed microRNAs in blood samples of patients affected by glioma. We studied the miRNAs' expression, by means of microarray and Real-Time PCR, in 30 blood samples from glioma patients and in 82 blood samples of patients suffering from: (a) various neurological disorders (n=30), (b) primary B-lymphoma of the Central Nervous System (PCNSL, n=36) and (c) secondary brain metastases (n=16). By quantitative real time reverse-transcriptase polymerase chain reaction (qRT-PCR), we identified significantly increased levels of two candidate biomarkers, miR-15b and miR-21, in blood of patients affected by gliomas. ROC analysis of miR-15b biomarker levels allowed to differentiate patients with tumour from patients without glioma. Furthermore, combined expression analyses of miR15b and miR-21 distinguished between patients with and without glioma (90% sensitivity and 100% specificity). In addition, a decrement in the expression levels of miR-16 characterized glioblastomas compared to low grade and anaplastic gliomas. In conclusion, this pilot study suggest that it's possible to identify the disease state by meaning miR-15b and miR-21 markers in blood, while miR-16 can be used to distinguish glioblastoma from other grade gliomas. They can potentially be used as biomarkers for non-invasive diagnosis of gliomas; further studies are mandatory to confirm our preliminary findings.

Published
2015
Full Text
View/download PDF

41. Transcriptome-based identification of new anti-inflammatory and vasodilating properties of the n-3 fatty acid docosahexaenoic acid in vascular endothelial cell under proinflammatory conditions [corrected].

Author

Massaro M, Martinelli R, Gatta V, Scoditti E, Pellegrino M, Carluccio MA, Calabriso N, Buonomo T, Stuppia L, Storelli C, and De Caterina R

Subjects
CARD Signaling Adaptor Proteins genetics, CARD Signaling Adaptor Proteins metabolism, CD47 Antigen genetics, CD47 Antigen metabolism, Gene Expression Profiling, Gene Expression Regulation drug effects, Gene Knockdown Techniques, Gene Regulatory Networks, Guanylate Cyclase genetics, Guanylate Cyclase metabolism, Human Umbilical Vein Endothelial Cells, Humans, Interleukin-1beta pharmacology, Signal Transduction drug effects, Docosahexaenoic Acids pharmacology, Endothelial Cells drug effects, Endothelial Cells metabolism, Inflammation Mediators pharmacology, Transcriptome, Vasodilator Agents pharmacology
Abstract

Scope: High intakes of n-3 fatty acids exert anti-inflammatory effects and cardiovascular protection, but the underlying molecular basis is incompletely defined. By genome-wide analysis we searched for novel effects of docosahexaenoic acid (DHA) on gene expression and pathways in human vascular endothelium under pro-inflammatory conditions., Methods and Results: Human umbilical vein endothelial cells were treated with DHA and then stimulated with interleukin(IL)-1β. Total RNA was extracted, and gene expression examined by DNA microarray. DHA alone altered the expression of 188 genes, decreasing 92 and increasing 96. IL-1β changed the expression of 2031 genes, decreasing 997 and increasing 1034. Treatment with DHA before stimulation significantly affected the expression of 116 IL-1β-deregulated genes, counter-regulating the expression of 55 genes among those decreased and of 61 among those increased. Functional and network analyses identified immunological, inflammatory and metabolic pathways as the most affected. Newly identified DHA-regulated genes are involved in stemness, cellular growth, cardiovascular system function and cancer, and included cytochrome p450 4F2(CYP4F2), transforming growth factor(TGF)-β2, Cluster of Differentiation (CD)47, caspase recruitment domain(CARD)11 and phosphodiesterase(PDE)5α., Conclusions: Endothelial exposure to DHA regulates novel genes and related pathways. Such unbiased identification should increase our understanding of mechanisms by which n-3 fatty acids affect human diseases.

Published
2015
Full Text
View/download PDF

42. Additive regulation of adiponectin expression by the mediterranean diet olive oil components oleic Acid and hydroxytyrosol in human adipocytes.

Author

Scoditti E, Massaro M, Carluccio MA, Pellegrino M, Wabitsch M, Calabriso N, Storelli C, and De Caterina R

Subjects
3T3-L1 Cells, Adipocytes metabolism, Animals, Down-Regulation drug effects, Drug Synergism, Enzyme Activation drug effects, Humans, JNK Mitogen-Activated Protein Kinases metabolism, Mice, PPAR gamma genetics, PPAR gamma metabolism, Phenylethyl Alcohol pharmacology, Tumor Necrosis Factor-alpha pharmacology, Adipocytes drug effects, Adiponectin genetics, Diet, Mediterranean, Gene Expression Regulation drug effects, Oleic Acid pharmacology, Olive Oil chemistry, Phenylethyl Alcohol analogs & derivatives
Abstract

Adiponectin, an adipocyte-derived insulin-sensitizing and anti-inflammatory hormone, is suppressed in obesity through mechanisms involving chronic inflammation and oxidative stress. Olive oil consumption is associated with beneficial cardiometabolic actions, with possible contributions from the antioxidant phenol hydroxytyrosol (HT) and the monounsaturated fatty acid oleic acid (OA, 18:1n-9 cis), both possessing anti-inflammatory and vasculo-protective properties. We determined the effects of HT and OA, alone and in combination, on adiponectin expression in human and murine adipocytes under pro-inflammatory conditions induced by the cytokine tumor necrosis factor(TNF)-α. We used human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes and murine 3T3-L1 adipocytes as cell model systems, and pretreated them with 1-100 μmol/L OA, 0.1-20 μmol/L HT or OA plus HT combination before stimulation with 10 ng/mL TNF-α. OA or HT significantly (P<0.05) prevented TNF-α-induced suppression of total adiponectin secretion (by 42% compared with TNF-α alone) as well as mRNA levels (by 30% compared with TNF-α alone). HT and OA also prevented-by 35%-TNF-α-induced downregulation of peroxisome proliferator-activated receptor PPARγ. Co-treatment with HT and OA restored adiponectin and PPARγ expression in an additive manner compared with single treatments. Exploring the activation of JNK, which is crucial for both adiponectin and PPARγ suppression by TNF-α, we found that HT and OA additively attenuated TNF-α-stimulated JNK phosphorylation (up to 55% inhibition). In conclusion, the virgin olive oil components OA and HT, at nutritionally relevant concentrations, have additive effects in preventing adiponectin downregulation in inflamed adipocytes through an attenuation of JNK-mediated PPARγ suppression.

Published
2015
Full Text
View/download PDF

43. Antitumor activity of the dietary diterpene carnosol against a panel of human cancer cell lines.

Author

Vergara D, Simeone P, Bettini S, Tinelli A, Valli L, Storelli C, Leo S, Santino A, and Maffia M

Subjects
Caco-2 Cells, Cell Adhesion drug effects, Cell Line, Tumor, Cell Proliferation drug effects, Cell Survival drug effects, Humans, MCF-7 Cells, Phytochemicals pharmacology, Abietanes pharmacology, Antineoplastic Agents pharmacology
Abstract

Dietary phytochemicals found in vegetables and fruits consist of a wide variety of biologically active compounds with anti-carcinogenic activity. The aim of this study was to evaluate the antigrowth activity of carnosol, a dietary diterpene, as a single agent or in combination with other dietary phytochemicals or chemotherapeutic drugs against a panel of tumor cell lines. Carnosol decreased cell viability in human breast, ovarian, and intestinal tumor cell lines, and inhibited cancer cell adhesion on fibronectin and growth of cancer cells in suspension. Carnosol also inhibited EGF-induced epithelial mesenchymal transition in ovarian cancer cells. The combination treatment with other dietary phytochemicals increased the anti-proliferative activity of carnosol. The combination with curcumin resulted in a synergistic reduction of vitality in SKOV-3 and MDA-231 cells and potently inhibited viability of primary cancer cells isolated from the pleural fluid or ascites of patients with metastatic cancers. These results provide additional evidence about the anticancer role of carnosol and its potential in blocking the growth of tumor cells.

Published
2014
Full Text
View/download PDF

44. Teleost fish models in membrane transport research: the PEPT1(SLC15A1) H+-oligopeptide transporter as a case study.

Author

Romano A, Barca A, Storelli C, and Verri T

Subjects
Animals, Base Sequence, Molecular Sequence Data, Peptide Transporter 1, Species Specificity, Structure-Activity Relationship, Tissue Distribution, Zebrafish Proteins, Fishes classification, Fishes genetics, Genetic Variation genetics, Membrane Transport Proteins genetics, Organ Specificity genetics, Symporters genetics
Abstract

Human genes for passive, ion-coupled transporters and exchangers are included in the so-called solute carrier (SLC) gene series, to date consisting of 52 families and 398 genes. Teleost fish genes for SLC proteins have also been described in the last two decades, and catalogued in preliminary SLC-like form in 50 families and at least 338 genes after systematic GenBank database mining (December 2010-March 2011). When the kinetic properties of the expressed proteins are studied in detail, teleost fish SLC transporters always reveal extraordinary 'molecular diversity' with respect to the mammalian counterparts, which reflects peculiar adaptation of the protein to the physiology of the species and/or to the environment where the species lives. In the case of the H+ -oligopeptide transporter PEPT1(SLC15A1), comparative analysis of diverse teleost fish orthologs has shown that the protein may exhibit very eccentric properties in terms of pH dependence (e.g., the adaptation of zebrafish PEPT1 to alkaline pH), temperature dependence (e.g., the adaptation of icefish PEPT1 to sub-zero temperatures) and/or substrate specificity (e.g., the species-specificity of PEPT1 for the uptake of l-lysine-containing peptides). The revelation of such peculiarities is providing new contributions to the discussion on PEPT1 in both basic (e.g., molecular structure-function analyses) and applied research (e.g., optimizing diets to enhance growth of commercially valuable fish).

Published
2014
Full Text
View/download PDF

45. Hydroxytyrosol suppresses MMP-9 and COX-2 activity and expression in activated human monocytes via PKCα and PKCβ1 inhibition.

Author

Scoditti E, Nestola A, Massaro M, Calabriso N, Storelli C, De Caterina R, and Carluccio MA

Subjects
Diet, Mediterranean, Down-Regulation, Enzyme Activation, Humans, Inflammation, Leukocytes, Mononuclear drug effects, Macrophages metabolism, Monocytes cytology, NF-kappa B p50 Subunit metabolism, Olive Oil, Oxidation-Reduction, Oxidative Stress, Phenylethyl Alcohol chemistry, Phorbol Esters, Plant Oils chemistry, Polyphenols chemistry, Signal Transduction, U937 Cells, Cyclooxygenase 2 metabolism, Gene Expression Regulation, Enzymologic drug effects, Matrix Metalloproteinase 9 metabolism, Monocytes enzymology, Phenylethyl Alcohol analogs & derivatives, Protein Kinase C beta metabolism, Protein Kinase C-alpha metabolism
Abstract

Objective: Hydroxytyrosol (HT), the major olive oil antioxidant polyphenol in cardioprotective Mediterranean diets, is endowed with anti-inflammatory and anti-atherosclerotic activity. The production of cyclooxygenase (COX)-2-dependent inflammatory eicosanoids and the functionally linked release of matrix metalloproteinase (MMP)-9 by macrophages likely contribute to plaque instability leading to acute coronary events. Objective of the study was to examine the HT effects on inflammatory markers in human activated monocytes, including MMP-9 and COX-2 activity and expression and explore HT underlying mechanisms., Methods and Results: Human peripheral blood mononuclear cells (PBMC) and U937 monocytes were treated with 1-10 μmol/L HT before activation with phorbol myristate acetate (PMA). HT blunted monocyte matrix invasive potential and reduced MMP-9 release and expression at zymography, ELISA and RT-PCR, with an IC50 = 10 μmol/L ( P< 0.05), without affecting tissue inhibitor of metalloproteinase (TIMP)-1. Moreover, HT inhibited prostaglandin (PG)E2 production and COX-2 expression, without affecting COX-1. These effects were mediated by inhibition of transcription factor nuclear factor (NF)-κB and protein kinase C (PKC)α and PKCβ1 activation., Conclusion: HT, at nutritionally relevant concentrations, reduces MMP-9 and COX-2 induction in activated human monocytes via PKCα and PKCβ1 inhibition, thus featuring novel anti-inflammatory properties. Overall, such results contribute to explaining the vascular protective effects by olive oil polyphenols in Mediterranean diets., (Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.)

Published
2014
Full Text
View/download PDF

46. Anti-aggregating effect of the naturally occurring dipeptide carnosine on aβ1-42 fibril formation.

Author

Aloisi A, Barca A, Romano A, Guerrieri S, Storelli C, Rinaldi R, and Verri T

Subjects
Amyloid chemistry, Amyloid metabolism, Amyloid ultrastructure, Amyloid beta-Peptides chemistry, Carnosine chemistry, Dose-Response Relationship, Drug, Humans, Models, Molecular, Molecular Conformation, Molecular Docking Simulation, Protein Binding, Amyloid beta-Peptides metabolism, Carnosine pharmacology, Protein Multimerization drug effects
Abstract

Carnosine is an endogenous dipeptide abundant in the central nervous system, where by acting as intracellular pH buffering molecule, Zn/Cu ion chelator, antioxidant and anti-crosslinking agent, it exerts a well-recognized multi-protective homeostatic function for neuronal and non-neuronal cells. Carnosine seems to counteract proteotoxicity and protein accumulation in neurodegenerative conditions, such as Alzheimer's Disease (AD). However, its direct impact on the dynamics of AD-related fibril formation remains uninvestigated. We considered the effects of carnosine on the formation of fibrils/aggregates of the amyloidogenic peptide fragment Aβ1-42, a major hallmark of AD injury. Atomic force microscopy and thioflavin T assays showed inhibition of Aβ1-42 fibrillogenesis in vitro and differences in the aggregation state of Aβ1-42 small pre-fibrillar structures (monomers and small oligomers) in the presence of carnosine. in silico molecular docking supported the experimental data, calculating possible conformational carnosine/Aβ1-42 interactions. Overall, our results suggest an effective role of carnosine against Aβ1-42 aggregation.

Published
2013
Full Text
View/download PDF

47. Protein cold adaptation strategy via a unique seven-amino acid domain in the icefish (Chionodraco hamatus) PEPT1 transporter.

Author

Rizzello A, Romano A, Kottra G, Acierno R, Storelli C, Verri T, Daniel H, and Maffia M

Subjects
Amino Acid Sequence, Animals, Base Sequence, Cloning, Molecular, Cluster Analysis, Models, Molecular, Molecular Sequence Data, Mutagenesis, Site-Directed, Patch-Clamp Techniques, Peptide Transporter 1, Phylogeny, Protein Structure, Tertiary genetics, Protein Structure, Tertiary physiology, Real-Time Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction, Sequence Analysis, DNA, Symporters genetics, Adaptation, Biological physiology, Cold Temperature, Perciformes physiology, Symporters physiology
Abstract

Adaptation of organisms to extreme environments requires proteins to work at thermodynamically unfavorable conditions. To adapt to subzero temperatures, proteins increase the flexibility of parts of, or even the whole, 3D structure to compensate for the lower thermal kinetic energy available at low temperatures. This may be achieved through single-site amino acid substitutions in regions of the protein that undergo large movements during the catalytic cycle, such as in enzymes or transporter proteins. Other strategies of cold adaptation involving changes in the primary amino acid sequence have not been documented yet. In Antarctic icefish (Chionodraco hamatus) peptide transporter 1 (PEPT1), the first transporter cloned from a vertebrate living at subzero temperatures, we came upon a unique principle of cold adaptation. A de novo domain composed of one to six repeats of seven amino acids (VDMSRKS), placed as an extra stretch in the cytosolic COOH-terminal region, contributed per se to cold adaptation. VDMSRKS was in a protein region uninvolved in transport activity and, notably, when transferred to the COOH terminus of a warm-adapted (rabbit) PEPT1, it conferred cold adaptation to the receiving protein. Overall, we provide a paradigm for protein cold adaptation that relies on insertion of a unique domain that confers greater affinity and maximal transport rates at low temperatures. Due to its ability to transfer a thermal trait, the VDMSRKS domain represents a useful tool for future cell biology or biotechnological applications.

Published
2013
Full Text
View/download PDF

48. Comparative analysis and functional mapping of SACS mutations reveal novel insights into sacsin repeated architecture.

Author

Romano A, Tessa A, Barca A, Fattori F, de Leva MF, Terracciano A, Storelli C, Santorelli FM, and Verri T

Subjects
Computational Biology, Exons, Heat-Shock Proteins metabolism, Humans, Mutation, Phenotype, Phylogeny, Polymorphism, Single Nucleotide, RNA, Messenger genetics, RNA, Messenger metabolism, Sequence Alignment, Sequence Analysis, DNA, Spinocerebellar Ataxias genetics, Chromosome Mapping, Heat-Shock Proteins genetics, Muscle Spasticity genetics, Spinocerebellar Ataxias congenital
Abstract

Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is a neurological disease with mutations in SACS, encoding sacsin, a multidomain protein of 4,579 amino acids. The large size of SACS and its translated protein has hindered biochemical analysis of ARSACS, and how mutant sacsins lead to disease remains largely unknown. Three repeated sequences, called sacsin repeating region (SRR) supradomains, have been recognized, which contribute to sacsin chaperone-like activity. We found that the three SRRs are much larger (≥1,100 residues) than previously described, and organized in discrete subrepeats. We named the large repeated regions Sacsin Internal RePeaTs (SIRPT1, SIRPT2, and SIRPT3) and the subrepeats sr1, sr2, sr3, and srX. Comparative analysis of vertebrate sacsins in combination with fine positional mapping of a set of human mutations revealed that sr1, sr2, sr3, and srX are functional. Notably, the position of the pathogenic mutations in sr1, sr2, sr3, and srX appeared to be related to the severity of the clinical phenotype, as assessed by defining a severity scoring system. Our results suggest that the relative position of mutations in subrepeats will variably influence sacsin dysfunction. The characterization of the specific role of each repeated region will help in developing a comprehensive and integrated pathophysiological model of function for sacsin., (© 2012 Wiley Periodicals, Inc.)

Published
2013
Full Text
View/download PDF

49. Dipyridamole decreases inflammatory metalloproteinase-9 expression and release by human monocytes.

Author

Massaro M, Scoditti E, Carluccio MA, Pellegrino M, Calabriso N, Storelli C, Martines G, and De Caterina R

Subjects
Cyclic AMP metabolism, Cyclic GMP metabolism, Dose-Response Relationship, Drug, Down-Regulation, Humans, I-kappa B Proteins metabolism, Matrix Metalloproteinase 9 genetics, Monocytes enzymology, Monocytes immunology, NF-KappaB Inhibitor alpha, RNA, Messenger metabolism, Signal Transduction drug effects, Time Factors, Tissue Inhibitor of Metalloproteinase-1 metabolism, Transcription Factor AP-1 metabolism, Transcription Factor RelA metabolism, Tumor Necrosis Factor-alpha metabolism, U937 Cells, p38 Mitogen-Activated Protein Kinases metabolism, Anti-Inflammatory Agents pharmacology, Dipyridamole pharmacology, Inflammation Mediators metabolism, Matrix Metalloproteinase 9 metabolism, Monocytes drug effects
Abstract

Matrix metalloproteinase (MMP)-9 plays an important role in stroke by accelerating matrix degradation, disrupting the blood-brain barrier and increasing infarct size. Dipyridamole is an antiplatelet agent with recognised benefits in ischaemic stroke prevention. In addition to its antiplatelet properties, recent studies have reported that dipyridamole also features anti-inflammatory and anti-oxidant properties. We therefore investigated whether dipyridamole can ameliorate the proinflammatory profile of human monocytes, a source of MMP-9 in stroke, in terms of regulation of MMP-9 activity and expression, and explored underlying mechanisms. Human peripheral blood mononuclear cells (PBMC) and U937 cells were treated with increasing concentrations of dipyridamole (up to 10 µg/ml) for 60 minutes before stimulation with tumour necrosis factor (TNF)-α or phorbol myristate acetate (PMA). Exposure of PBMC and U937 to dipyridamole reduced TNF-α- and PMA-induced MMP-9 activity and protein release as well as MMP-9 mRNA, without significantly affecting the release of TIMP-1. This inhibitory effect was independent of dipyridamole-induced cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) increase. Correspondingly, dipyridamole also significantly inhibited TNF-α-induced nuclear factor (NF)-κB activation and nuclear translocation of the p65 NF-κB subunit through a mechanism involving the inhibition of IkBα degradation and p38 MAPK activation. In conclusion, dipyridamole, at therapeutically achievable concentrations, reduces the expression and release of MMP-9 through a mechanism involving p38 MAPK and NF-κB inhibition. These results indicate that dipyridamole exerts anti-inflammatory properties in human monocytes that may favourably contribute to its actions in the secondary prevention of stroke, independent of its antiplatelet properties.

Published
2013
Full Text
View/download PDF

50. Mediterranean diet polyphenols reduce inflammatory angiogenesis through MMP-9 and COX-2 inhibition in human vascular endothelial cells: a potentially protective mechanism in atherosclerotic vascular disease and cancer.

Author

Scoditti E, Calabriso N, Massaro M, Pellegrino M, Storelli C, Martines G, De Caterina R, and Carluccio MA

Subjects
Antioxidants pharmacology, Antioxidants therapeutic use, Cyclooxygenase 2 Inhibitors pharmacology, Cyclooxygenase 2 Inhibitors therapeutic use, Gene Expression Regulation, Enzymologic drug effects, Human Umbilical Vein Endothelial Cells enzymology, Human Umbilical Vein Endothelial Cells metabolism, Humans, Inflammation physiopathology, Matrix Metalloproteinase Inhibitors pharmacology, Matrix Metalloproteinase Inhibitors therapeutic use, NF-kappa B metabolism, Neovascularization, Pathologic drug therapy, Neovascularization, Pathologic enzymology, Neovascularization, Pathologic metabolism, Neovascularization, Pathologic pathology, Olive Oil, Plant Oils chemistry, Polyphenols therapeutic use, Reactive Oxygen Species metabolism, Tetradecanoylphorbol Acetate pharmacology, Wine analysis, Atherosclerosis prevention & control, Cyclooxygenase 2 metabolism, Diet, Mediterranean, Human Umbilical Vein Endothelial Cells drug effects, Matrix Metalloproteinase 9 metabolism, Neoplasms prevention & control, Polyphenols pharmacology
Abstract

Diets with high content of antioxidant polyphenols are associated with low prevalence of cardiovascular diseases and cancer. Inflammatory angiogenesis is a key pathogenic process both in cancer and atherosclerosis, and is tightly regulated by the proinflammatory enzyme cyclooxygenase (COX)-2 and the matrix degrading enzymes matrix metalloproteinases (MMPs). We studied the effects of antioxidant polyphenols from virgin olive oil (oleuropein and hydroxytyrosol) and red wine (resveratrol and quercetin) on endothelial cell angiogenic response in vitro, and explored underlying mechanisms. Cultured endothelial cells were pre-incubated with 0.1-50 μmol/L polyphenols before stimulation with phorbol myristate acetate (PMA). All tested polyphenols reduced endothelial cell tube formation on matrigel and migration in wound healing assays. The reduced angiogenesis was associated with the inhibition of PMA-induced COX-2 protein expression and prostanoid production, as well as MMP-9 protein release and gelatinolytic activity. These effects were accompanied by a significant reduction in the stimulated intracellular reactive oxygen species levels and in the activation of the redox-sensitive transcription factor nuclear factor (NF)-κB. Our findings reveal that olive oil and red wine polyphenols reduce inflammatory angiogenesis in cultured endothelial cells, through MMP-9 and COX-2 inhibition, supporting a potential protective role for dietary polyphenols in atherosclerotic vascular disease and cancer., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Published
2012
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results