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14 results on '"O. Duicu"'

1. Poster session 3Cell growth, differentiation and stem cells - Heart511The role of the endocannabinoid system in modelling muscular dystrophy cardiac disease with induced pluripotent stem cells.512An emerging role of T lymphocytes in cardiac regenerative processes in heart failure due to dilated cardiomyopathy513Canonical wnt signaling reverses the ‘aged/senescent’ human endogenous cardiac stem cell phenotype514Hippo signalling modulates survival of human induced pluripotent stem cell-derived cardiomyocytes515Biocompatibility of mesenchymal stem cells with a spider silk matrix and its potential use as scaffold for cardiac tissue regeneration516A snapshot of genome-wide transcription in human induced pluripotent stem cell-derived hepatocyte-like cells (iPSC-HLCs)517Can NOS/sGC/cGK1 pathway trigger the differentiation and maturation of mouse embryonic stem cells (ESCs)?518Introduction of external Ik1 to human-induced pluripotent stem cell-derived cardiomyocytes via Ik1-expressing HEK293519Cell therapy of the heart studied using adult myocardial slices in vitro520Enhancement of the paracrine potential of human adipose derived stem cells when cultured as spheroid bodies521Mechanosensitivity of cardiomyocyte progenitor cells: the strain response in 2D and 3D environments522The effect of the vascular-like network on the maturation of the human induced pluripotent stem cell derived cardiomyocytes.Transcriptional control and RNA species - Heart525Gene expression regulation in heart failure: from pathobiology to bioinformatics526Human transcriptome in idiopathic dilated cardiomyopathy - a novel high throughput screening527A high-throghput approach unveils putative miRNA-mediated mitochondria-targeted cardioprotective circuits activated by T3 in the post ischemia reperfusion setting528The effect of uraemia on the expression of miR-212/132 and the calcineurin pathway in the rat heartCytokines and cellular inflammation - Heart531Lack of growth differentiation factor 15 aggravates adverse cardiac remodeling upon pressure-overload in mice532Blocking heteromerization of platelet chemokines ccl5 and cxcl4 reduces inflammation and preserves heart function after myocardial infarction533Is there an association between low-dose aspirin use and clinical outcome in HFPEF? Implications of modulating monocyte function and inflammatory mediator release534N-terminal truncated intracellular matrix metalloproteinase-2 expression in diabetic heart.535Expression of CD39 and CD73 on peripheral T-cell subsets in calcific aortic stenosis536Mast cells in the atrial myocardium of patients with atrial fibrillation: a comparison with patients in sinus rhythm539Characteristics of the inflammatory response in patients with coronary artery disease and arterial hypertension540Pro-inflammatory cytokines as cardiovascular events predictors in rheumatoid arthritis and asymptomatic atherosclerosis541Characterization of FVB/N murinic bone marrow-derived macrophage polarization into M1 and M2 phenotypes542The biological expression and thoracic anterior pain syndromeSignal transduction - Heart545The association of heat shock protein 90 and TGFbeta receptor I is involved in collagen production during cardiac remodelling in aortic-banded mice546Loss of the inhibitory GalphaO protein in the rostral ventrolateral medulla of the brainstem leads to abnormalities in cardiovascular reflexes and altered ventricular excitablitiy547Selenoprotein P regulates pressure overload-induced cardiac remodeling548Study of adenylyl cyclase activity in erythrocyte membranes in patients with chronic heart failure549Direct thrombin inhibitors inhibit atrial myocardium hypertrophy in a rat model of heart failure and atrial remodeling550Tissue factor / FVIIa transactivates the IGF-1R by a Src-dependent phosphorylation of caveolin-1551Notch signaling is differently altered in endothelial and smooth muscle cells of ascending aortic aneurysm patients552Frizzled 5 expression is essential for endothelial proliferation and migration553Modulation of vascular function and ROS production by novel synthetic benzopyran analogues in diabetes mellitusExtracellular matrix and fibrosis - Heart556Cardiac fibroblasts as inflammatory supporter cells trigger cardiac inflammation in heart failure557A role for galectin-3 in calcific aortic valve stenosis558Omega-3 polyunsaturated fatty acids- can they decrease risk for ventricular fibrillation?559Serum levels of elastin derived peptides and circulating elastin-antielastin immune complexes in sera of patients with coronary artery disease560Endocardial fibroelastosis is secondary to hemodynamic alterations in the chick model of hypoplastic left heart syndrome561Dynamics of serum levels of matrix metalloproteinases in primary anterior STEMI patients564Deletion of the alpha-7 nicotinic acetylcholine receptor changes the vascular remodeling induced by transverse aortic constriction in mice.565Extracellular matrix remodelling in response to venous hypertension: proteomics of human varicose veinsIon channels, ion exchangers and cellular electrophysiology - Heart568Microtubule-associated protein RP/EB family member 1 modulates sodium channel trafficking and cardiac conduction569Investigation of electrophysiological abnormalities in a rabbit athlete's heart model570Upregulation of expression of multiple genes in the atrioventricular node of streptozotocin-induced diabetic rat571miR-1 as a regulator of sinoatrial rhythm in endurance training adaptation572Selective sodium-calcium exchanger inhibition reduces myocardial dysfunction associated with hypokalaemia and ventricular fibrillation573Effect of racemic and levo-methadone on action potential of human ventricular cardiomyocytes574Acute temperature effects on the chick embryonic heart functionVasculogenesis, angiogenesis and arteriogenesis577Clinical improvement and enhanced collateral vessel growth after monocyte transplantation in mice578The role of HIF-1 alpha, VEGF and obstructive sleep apnoea in the development of coronary collateral circulation579Initiating cardiac repair with a trans-coronary sinus catheter intervention in an ischemia/reperfusion porcine animal model580Early adaptation of pre-existing collaterals after acute arteriolar and venular microocclusion: an in vivo study in chick chorioallantoic membraneEndothelium583EDH-type responses to the activator of potassium KCa2.3 and KCa3.1 channels SKA-31 in the small mesenteric artery from spontaneously hypertensive rats584The peculiarities of endothelial dysfunction in patients with chronic renocardial syndrome585Endothelial dysfunction, atherosclerosis of the carotid arteries and level of leptin in patient with coronary heart disease in combination with hepatic steatosis depend from body mass index.586Role of non-coding RNAs in thoracic aortic aneurysm associated with bicuspid aortic valve587Cigarette smoke extract abrogates atheroprotective effects of high laminar flow on endothelial function588The prognostic value of anti-connective tissue antibodies in coronary heart disease and asymptomatic atherosclerosis589Novel potential properties of bioactive peptides from spanish dry-cured ham on the endothelium.Lipids592Intermediate density lipoprotein is associated with monocyte subset distribution in patients with stable atherosclerosis593The characteristics of dyslipidemia in rheumatoid arthritisAtherosclerosis596Macrophages differentiated in vitro are heterogeneous: morphological and functional profile in patients with coronary artery disease597Palmitoylethanolamide promotes anti-inflammatory phenotype of macrophages and attenuates plaque formation in ApoE-/- mice598Amiodarone versus esmolol in the perioperative period: an in vitro study of coronary artery bypass grafts599BMPRII signaling of fibrocytes, a mesenchymal progenitor cell population, is increased in STEMI and dyslipidemia600The characteristics of atherogenesis and systemic inflammation in rheumatoid arthritis601Role of adenosine-to-inosine RNA editing in human atherosclerosis602Presence of bacterial DNA in thrombus aspirates of patients with myocardial infarction603Novel E-selectin binding polymers reduce atherosclerotic lesions in ApoE(-/-) mice604Differential expression of the plasminogen receptor Plg-RKT in monocyte and macrophage subsets - possible functional consequences in atherogenesis605Apelin-13 treatment enhances the stability of atherosclerotic plaques606Mast cells are increased in the media of coronary lesions in patients with myocardial infarction and favor atherosclerotic plaque instability607Association of neutrophil to lymphocyte ratio with presence of isolated coronary artery ectasiaCalcium fluxes and excitation-contraction coupling610The coxsackie- and adenovirus receptor (CAR) regulates calcium homeostasis in the developing heart611HMW-AGEs application acutely reduces ICaL in adult cardiomyocytes612Measuring electrical conductibility of cardiac T-tubular systems613Postnatal development of cardiac excitation-contraction coupling in rats614Role of altered Ca2+ homeostasis during adverse cardiac remodeling after ischemia/reperfusion615Experimental study of sarcoplasmic reticulum dysfunction and energetic metabolism in failing myocardium associated with diabetes mellitusHibernation, stunning and preconditioning618Volatile anesthetic preconditioning attenuates ischemic-reperfusion injury in type II diabetic patients undergoing on-pump heart surgery619The effect of early and delayed phase of remote ischemic preconditioning on ischemia-reperfusion injury in the isolated hearts of healthy and diabetic rats620Post-conditioning with 1668-thioate leads to attenuation of the inflammatory response and remodeling with less fibrosis and better left ventricular function in a murine model of myocardial infarction621Maturation-related changes in response to ischemia-reperfusion injury and in effects of classical ischemic preconditioning and remote preconditioningMitochondria and energetics624Phase changes in myocardial mitochondrial respiration caused by hypoxic preconditioning or periodic hypoxic training625Desmin mutations depress mitochondrial metabolism626Methylene blue modulates mitochondrial function and monoamine oxidases-related ROS production in diabetic rat hearts627Doxorubicin modulates the real-time oxygen consumption rate of freshly isolated adult rat and human ventricular cardiomyocytesCardiomyopathies and fibrosis630Effects of genetic or pharmacologic inhibition of the ubiquitin/proteasome system on myocardial proteostasis and cardiac function631Suppression of Wnt signalling in a desmoglein-2 transgenic mouse model for arrhythmogenic cardiomyopathy632Cold-induced cardiac hypertrophy is reversed after thermo-neutral deacclimatization633CD45 is a sensitive marker to diagnose lymphocytic myocarditis in endomyocardial biopsies of living patients and in autopsies634Atrial epicardial adipose tissue derives from epicardial progenitors635Caloric restriction ameliorates cardiac function, sympathetic cardiac innervation and beta-adrenergic receptor signaling in an experimental model of post-ischemic heart failure636High fat diet improves cardiac remodelling and function after extensive myocardial infarction in mice637Epigenetic therapy reduces cardiac hypertrophy in murine models of heart failure638Imbalance of the VHL/HIF signaling in WT1+ Epicardial Progenitors results in coronary vascular defects, fibrosis and cardiac hypertrophy639Diastolic dysfunction is the first stage of the developing heart failure640Colchicine aggravates coxsackievirus B3 infection in miceArterial and pulmonary hypertension642Osteopontin as a marker of pulmonary hypertension in patients with coronary heart disease combined with chronic obstructive pulmonary disease643Myocardial dynamic stiffness is increased in experimental pulmonary hypertension partly due to incomplete relaxation644Hypotensive effect of quercetin is possibly mediated by down-regulation of immunotroteasome subunits in aorta of spontaneously hypertensive rats645Urocortin-2 improves right ventricular function and attenuates experimental pulmonary arterial hypertension646A preclinical evaluation of the anti-hypertensive properties of an aqueous extract of Agathosma (Buchu)Biomarkers648The adiponectin level in hypertensive females with rheumatoid arthritis and its relationship with subclinical atherosclerosis649Markers for identification of renal dysfunction in the patients with chronic heart failure650cardio-hepatic syndromes in chronic heart failure: North Africa profile651To study other biomarkers that assess during myocardial infarction652Interconnections of apelin levels with parameters of lipid metabolism in hypertension patients653Plasma proteomics in hypertension: prediction and follow-up of albuminuria during chronic renin-angiotensin system suppression654Soluble RAGE levels in plasma of patients with cerebrovascular events

Author

C Falcone, M Baldan Martin, K Yushko, SUMIYA Tserendavaa, I Nassiri, U Kamilova, O Sirenko, B Huisamen, R Adao, S Goncharov, WJ Van Der Laarse, O Hetman, RW Emmens, VI Kapelko, I Menendez-Montes, A Russell-Hallinan, O Tsoref, C De Lucia, N Suffee, L Woudstra, C Ruperez, A Lorenzon, T Zaglia, JM Elder, OANA M Duicu, N Smolina, VI Portnichenko, L Griecsova, GD Duerr, M Murarikova, T Sosorburam, D Kondrat'eva, A Dominguez, A Zahradnikova, M Scardigli, D Deluyker, C Matthaeus, MNS Shaaban, WW Fuijkschot, RA Fraga-Silva, B Thaler, P Pinon, K Stellos, J Starodubova, T Hofbauer, D Ozkaramanli Gur, P Rinne, S Fiorelli, KA Krychtiuk, SM Martinez Sanchez, AR Babaeva, H Morawietz, A Bhattachariya, M Grechanyk, A Maslenko, M Kloza, W Xiang, C Nebert, MA Abela, M Wagner, F Vostarek, L Diolaiuti, J Prorok, A Gualdoni, FC Howarth, P Kui, V Portero, M Lynch, FP Neto, V Ryabov, D Sedmera, A Nikolov, B Bacova, R Sadaba, D Lindner, D Muntean, MM Brandt, DA Kostina, M Aberg, C Jumeau, S Usui, R Ang, RG Garcia, D Munteanu, M DE C Santuchi, NP Korzhenkov, NA Musikhina, T Kucera, A Golovkin, H W Lee, N Glezeva, T Vajen, SCA De Jager, M Sarkozy, F Forini, A Chaloupka, C Schiano, M Pekkanen-Mattila, NAM Bax, C Sid-Otmane, F Perbellini, A Costa, V Spinelli, LE Viiri, L Fuentes, G Foldes, FC Lewis, T Kulikova, A Gowran, V Vigorelli, P Nigro, G Pompilio, O Stepanova, M Valikhov, A Samko, V Masenko, S Tereschenko, T Teoh, E Domenjo-Vila, T Theologou, M Field, W Awad, M Yasin, B Nadal-Ginard, GM Ellison-Hughes, N Hellen, O Vittay, SE Harding, L Gomez-Cid, ME Fernandez-Santos, S Suarez-Sancho, V Plasencia, A Climent, R Sanz-Ruiz, M Hedhammar, F Atienza, F Fernandez-Aviles, M Kiamehr, M Oittinen, KM Viiri, M Kaikkonen, K Aalto-Setala, A Laurino, L Sartiani, A Vona, M Zanardelli, E Cerbai, P Failli, MP Hortigon-Vinagre, M Van Der Heyden, FL Burton, GL Smith, S Watson, M Scigliano, S Tkach, S Alayoubi, CM Terracciano, HQ Ly, A Mauretti, MH Van Marion, MC Van Turnhout, DWJ Van Der Schaft, CM Sahlgren, MJ Goumans, CVC Bouten, H Vuorenpaa, K Penttinen, R Sarkanen, T Ylikomi, T Heinonen, V Grimaldi, M Aprile, R Esposito, C Maiello, A Soricelli, V Colantuoni, V Costa, A Ciccodicola, C Napoli, GC Rowe, K Johnson, ZP Arany, F Del Monte, R D'aurizio, C Kusmic, G Nicolini, M Baumgart, M Groth, N Ucciferri, G Iervasi, L Pitto, M Pipicz, R Gaspar, A Siska, I Foldesi, K Kiss, P Bencsik, T Thum, S Batkai, T Csont, JJ Haan, L Bosch, MAD Brans, SM Van De Weg, JC Deddens, SJ Lee, JPG Sluijter, G Pasterkamp, I Werner, D Projahn, M Staudt, A Curaj, TT Soenmez, S Simsekyilmaz, TM Hackeng, P Von Hundelshausen, RR Koenen, C Weber, EA Liehn, M Santos-Martinez, C Medina, C Watson, K Mcdonald, J Gilmer, M Ledwidge, SH Song, MY Lee, MH Park, JC Choi, JH Ahn, JS Park, JH Oh, JH Choi, HC Lee, KS Cha, TJ Hong, I Kudryavtsev, M Serebryakova, A Malashicheva, A Shishkova, E Zhiduleva, O Moiseeva, M Durisova, M Blaha, V Melenovsky, J Pirk, J Kautzner, TI Petelina, LI Gapon, EA Gorbatenko, YV Potolinskaya, EV Arkhipova, KS Solodenkova, MA Osadchuk, MF Dutra, FCB Oliveira, MM Silva, DG Passos-Silva, R Goncalves, RAS Santos, RF Da Silva, CM Gavrilescu, CM Paraschiv, P Manea, LC Strat, JMG Gomez, D Merino, MA Hurle, JF Nistal, A Aires, AL Cortajarena, AV Villar, J Abramowitz, L Birnbaumer, AV Gourine, A Tinker, M Takamura, S Takashima, O Inoue, H Misu, T Takamura, S Kaneko, TOHIRA Alieva, N Mougenot, M Dufilho, S Hatem, A Siegbahn, AS Kostina, VE Uspensky, OM Moiseeva, AA Kostareva, AB Malashicheva, CGM Van Dijk, I Chrifi, MC Verhaar, DJ Duncker, C Cheng, A Sturza, A Petrus, O Duicu, L Kiss, M Danila, I Baczko, N Jost, F Gotzhein, J Schon, M Schwarzl, S Hinrichs, S Blankenberg, U Volker, E Hammer, D Westermann, E Martinez-Martinez, V Arrieta, A Fernandez-Celis, L Jimenez-Alfaro, A Melero, V Alvarez-Asiain, V Cachofeiro, N Lopez-Andres, N Tribulova, G Wallukat, V Knezl, J Radosinska, M Barancik, I Tsinlikov, I Tsinlikova, G Nicoloff, A Blazhev, Z Pesevski, A Kvasilova, T Stopkova, A Eckhardt, C M Buffinton, O Nanka, M Kercheva, T Suslova, A Gusakova, T Ryabova, V Markov, R Karpov, H Seemann, TC Alcantara, SG Fonseca, J Barallobre-Barreiro, R Oklu, M Fava, F Baig, X Yin, H Albadawi, M Jahangiri, J Stoughton, M Mayr, SP Podliesna, CCV Veerman, AOV Verkerk, MK Klerk, EML Lodder, IM Mengarelli, CRB Bezzina, CAR Remme, H Takacs, A Polyak, N Morvay, I Lepran, L Tiszlavicz, N Nagy, B Ordog, A Farkas, T Forster, A Varro, AS Farkas, P Jayaprakash, K Parekh, Z Ferdous, M Oz, H Dobrzynski, TE Adrian, S Landi, M Bonzanni, A D'souza, M Boyett, A Bucchi, M Baruscotti, D Difrancesco, A Barbuti, K Oravecz, T Hezso, J Levijoki, P Pollesello, T Koskelainen, L Otsomaa, A S Farkas, JGY Papp, A Toth, K Acsai, L Dini, L Mazzoni, A Mugelli, J Svatunkova, C Deffge, C Baer, S Weinert, RC Braun-Dullaeus, J Herold, AC Cassar, GZ Zahra, EP Pllaha, PD Dingli, SM Montefort, RGX Xuereb, T Aschacher, B Messner, E Eichmair, W Mohl, B Reglin, W Rong, B Nitzsche, M Maibier, P Guimaraes, A Ruggeri, TW Secomb, AR Pries, M Baranowska-Kuczko, O Karpinska, M Kusaczuk, B Malinowska, H Kozlowska, N Demikhova, L Vynnychenko, O Prykhodko, N Grechanyk, A Kuryata, KA Cottrill, L Du, HM Bjorck, S Maleki, A Franco-Cereceda, SY Chan, P Eriksson, S Giebe, N Cockcroft, K Hewitt, M Brux, C Brunssen, AA Tarasov, SI Davidov, EA Reznikova, A Tapia Abellan, D Angosto Bazarra, P Pelegrin Vivancos, S Montoro Garcia, SP Kastl, T Pongratz, G Goliasch, L Gaspar, G Maurer, K Huber, E Dostal, S Pfaffenberger, S Oravec, J Wojta, WS Speidl, I Osipova, I Sopotova, S Eligini, N Cosentino, G Marenzi, E Tremoli, M Rami, L Ring, S Steffens, O Gur, S Gurkan, A Mangold, T Scherz, A Panzenboeck, N Staier, H Heidari, J Mueller, IM Lang, A Gatsiou, K Stamatelopoulos, L Perisic, D John, FF Lunella, U Hedin, A Zeiher, S Dimmeler, L Nunez, R Moure, G Marron-Linares, X Flores, G Aldama, J Salgado, R Calvino, M Tomas, G Bou, N Vazquez, M Hermida-Prieto, JM Vazquez-Rodriguez, U Amit, N Landa, D Kain, D Tyomkin, A David, J Leor, PJ Hohensinner, J Baumgartner, N Baik, LA Miles, H Seeman, F Montecucco, AR Da Silva, FP Costa-Fraga, L Anguenot, FP Mach, N Stergiopulos, K Kupreishvili, ABA Vonk, YM Smulders, VWM Van Hinsbergh, W Stooker, HWM Niessen, PAJ Krijnen, MM Ashmawy, MA Salama, MZ Elamrosy, R Juettner, F G Rathjen, V Bito, C Crocini, C Ferrantini, T Gabbrielli, L Silvestri, R Coppini, C Tesi, C Poggesi, FS Pavone, L Sacconi, K Mackova, I Zahradnik, I Diaz, E Sanchez De Rojas De Pedro, K Hmadcha, E Calderon Sanchez, JP Benitah, AM Gomez, T Smani, A Ordonez, SA Afanasiev, MV Egorova, SV Popov, P Wu Qing, X Cheng, S Carnicka, D Pancza, M Jasova, I Kancirova, M Ferko, T Ravingerova, S Wu, M Schneider, V Marggraf, L Verfuerth, S Frede, O Boehm, O Dewald, G Baumgarten, S-C Kim, V Farkasova, I Gablovsky, I Bernatova, V Nosar, A Portnychenko, T Drevytska, I Mankovska, V Gogvadze, T Sejersen, A Kostareva, A Wolf, A Privistirescu, P O ' Gara, JL Sanchez-Alonso, AR Lyon, V Prando, N Pianca, F Lo Verso, G Milan, P Pesce, M Sandri, M Mongillo, G Beffagna, G Poloni, E Dazzo, P Sabatelli, R Doliana, R Polishchuk, D Carnevale, G Lembo, P Bonaldo, P Braghetta, A Rampazzo, M Cairo, M Giralt, F Villarroya, A Planavila, PS Biesbroek, RWE Emmens, LJM Juffermans, AC Van Der Wall, AC Van Rossum, JWM Niessen, T Moor Morris, G Dilanian, P Farahmand, M Puceat, G Gambino, L Petraglia, A Elia, K Komici, GD Femminella, ML D'amico, G Pagano, A Cannavo, D Liccardo, WJ Koch, M Nolano, D Leosco, N Ferrara, G Rengo, R Neary, L Shiels, J Baugh, B Palacios, B Escobar, AV Alonso, G Guzman, J Ruiz-Cabello, LJ Jimenez-Borreguero, S Martin-Puig, VL Lakomkin, EV Lukoshkova, AA Abramov, VV Gramovich, ON Vyborov, VV Ermishkin, NA Undrovinas, VP Shirinsky, BJ Smilde, G Fong Hing, D Wouters, S Zeerleder, JL Murk, SM Van Ham, S Heymans, O Krakhmalova, D Van Groen, SJP Bogaards, I Schalij, GV Portnichenko, LV Tumanovska, YV Goshovska, TU Lapikova-Bryhinska, VS Nagibin, VE Dosenko, P Mendes-Ferreira, C Maia-Rocha, D Santos-Ribeiro, F Potus, S Breuils-Bonnet, S Provencher, S Bonnet, M Rademaker, AF Leite-Moreira, C Bras-Silva, J Lopes, O Kuryata, T Lusynets, I Alikulov, M Nourddine, L Azzouzi, R Habbal, ODKHUU Enkhtaivan, ZORIGO Shagdar, MUNKHZ Malchinkhuu, MUNLHZ Malchinkhuu, S Koval, T Starchenko, L Mourino-Alvarez, L Gonzalez-Calero, T Sastre-Oliva, JA Lopez, J Vazquez, G Alvarez-Llamas, LUIS M Ruilope, F De La Cuesta, MG Barderas, S Bozzini, A D'angelo, and G Pelissero

Subjects
Matrigel, Physiology, Chemistry, Physiology (medical), Cellular differentiation, Self-healing hydrogels, Endogenous regeneration, Mechanosensitive channels, Mechanotransduction, Progenitor cell, Cardiology and Cardiovascular Medicine, Regenerative medicine, Cell biology
Abstract

Purpose Cardiomyocytes progenitor cells (CMPCs) are a candidate cell source for cardiac regenerative therapy. To assess their full potential for cardiac regeneration, it is essential to know if and how CMPCs sense and respond to the three-dimensional (3D) environment and the mechanical stimuli provided by the beating heart. Therefore, we study the response to cyclic strain of undifferentiated and predifferentiated human CMPCs in a 2D environment, as well as CMPC responses to unidirectionally constrained versus stress-free (unconstrained) 3D environments. The latter responses were studied using a hydrogel system that allows for interaction of the cells with a simulated ‘host’ tissue. Methods To test mechanosensitivity of CMPCs in 2D and 3D environments, the response of L9TB CMPCs to uniaxial (cyclic) strain (10% with 0.5 Hz) was investigated. To represent the 3D environment, CMPCs were cultured in unidirectionally constrained and stress-free collagen/Matrigel hydrogels, where the constrainment provides a static strain to the cells. The cellular mechanoresponse to the applied (cyclic) strain was quantified by cellular re-orientation away from the strain direction (strain avoidance). Next to cellular re-orientation, the effect of strain on cell differentiation was analyzed. Results Our results indicate that while undifferentiated cells maintain their original orientation, upon early cardiomyogenic differentiation (predifferentiated) CMPCs exhibit a distinct strain avoidance response during 48hrs of cyclic straining in a 2D environment. In 3D unidirectionally constrained hydrogels, undifferentiated CMPCs retain their cardiomyogenic profile. CMPCs cultured in 3D collagen/Matrigel hydrogels respond to static mechanical strains as expected by cell alignment. Conclusions Our results suggest that CMPCs respond to the presence of mechanical stimuli, in this research mimicked by the application of uniaxial (cyclic) strain in 2D and 3D environments, suggesting that CMPCs are indeed mechanosensitive. Although in 2D environments, mechanosensitivity of the CMPCs is dependent on their differentiation status. Our findings provide the first understanding of the ability of human CMPCs to sense mechanical stimuli, which is the first initial step in mechanotransduction. Mechanotransduction is essential for optimal recruitment, migration, and mechanical integration of progenitor cells into the injured myocardium. Therefore, the presented results can contribute to enhance efficacy of current treatments of cardiac disease, as well as to develop novel endogenous regeneration strategies.

Published
2016
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2. 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
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3. A Comprehensive Assessment of Apigenin as an Antiproliferative, Proapoptotic, Antiangiogenic and Immunomodulatory Phytocompound.

Author

Ghițu A, Schwiebs A, Radeke HH, Avram S, Zupko I, Bor A, Pavel IZ, Dehelean CA, Oprean C, Bojin F, Farcas C, Soica C, Duicu O, and Danciu C

Subjects
Adenosine Triphosphate metabolism, Angiogenesis Inhibitors therapeutic use, Anti-Inflammatory Agents pharmacology, Anti-Inflammatory Agents therapeutic use, Antineoplastic Agents, Phytogenic therapeutic use, Apigenin therapeutic use, Apoptosis, Caspase 3 metabolism, Cell Cycle Checkpoints drug effects, Cell Line, Tumor, Cell Movement, Cell Proliferation, Cytokines metabolism, Dendritic Cells drug effects, Dendritic Cells metabolism, Humans, Immunologic Factors therapeutic use, Inflammation prevention & control, L-Lactate Dehydrogenase metabolism, Lipopolysaccharides, Magnoliopsida chemistry, Mitochondria drug effects, Mitochondria metabolism, Phytotherapy, Plant Extracts pharmacology, Plant Extracts therapeutic use, Angiogenesis Inhibitors pharmacology, Antineoplastic Agents, Phytogenic pharmacology, Apigenin pharmacology, Diet, Immunologic Factors pharmacology, Inflammation metabolism, Melanoma drug therapy, Melanoma metabolism, Melanoma pathology
Abstract

Apigenin (4',5,7-trihydroxyflavone) (Api) is an important component of the human diet, being distributed in a wide number of fruits, vegetables and herbs with the most important sources being represented by chamomile, celery, celeriac and parsley. This study was designed for a comprehensive evaluation of Api as an antiproliferative, proapoptotic, antiangiogenic and immunomodulatory phytocompound. In the set experimental conditions, Api presents antiproliferative activity against the A375 human melanoma cell line, a G2/M arrest of the cell cycle and cytotoxic events as revealed by the lactate dehydrogenase release. Caspase 3 activity was inversely proportional to the Api tested doses, namely 30 μM and 60 μM. Phenomena of early apoptosis, late apoptosis and necrosis following incubation with Api were detected by Annexin V-PI double staining. The flavone interfered with the mitochondrial respiration by modulating both glycolytic and mitochondrial pathways for ATP production. The metabolic activity of human dendritic cells (DCs) under LPS-activation was clearly attenuated by stimulation with high concentrations of Api. Il-6 and IL-10 secretion was almost completely blocked while TNF alpha secretion was reduced by about 60%. Api elicited antiangiogenic properties in a dose-dependent manner. Both concentrations of Api influenced tumour cell growth and migration, inducing a limited tumour area inside the application ring, associated with a low number of capillaries.

Published
2019
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4. Vitamin D improves vascular function and decreases monoamine oxidase A expression in experimental diabetes.

Author

Sturza A, Văduva A, Uțu D, Rațiu C, Pop N, Duicu O, Popoiu C, Boia E, Matusz P, Muntean DM, and Olariu S

Subjects
Animals, Aorta pathology, Diabetes Mellitus, Experimental pathology, Endothelial Cells pathology, Male, Rats, Rats, Wistar, Aorta enzymology, Calcitriol pharmacology, Diabetes Mellitus, Experimental enzymology, Endothelial Cells enzymology, Gene Expression Regulation, Enzymologic drug effects, Monoamine Oxidase biosynthesis
Abstract

The active form of vitamin D, 1,25-dihydroxycholecalciferol (1,25(OH) 2 D 3 ), was reported to improve vascular function in patients with diabetes, yet the underlying mechanisms remain to be fully elucidated. Monoamine oxidase (MAO), a mitochondrial enzyme, with two isoforms (A and B) that generates hydrogen peroxide (H 2 O 2 ) as by-product, has been recently reported to contribute to the pathogenesis of endothelial dysfunction in diabetes. The present study assessed the interaction between vitamin D and MAO in the vascular wall in the setting of type 1 experimental diabetes. To this aim, diabetes was induced in male Wistar rats via a single injection of streptozotocin (STZ, 50 mg/kg, IP) and 1 month later thoracic aortas were harvested and used for organ bath studies and H 2 O 2 measurements. MAO expression was assessed by immunohistochemistry and RT-PCR. Endothelial function was evaluated in isolated aortic rings in the absence vs. presence of 1,25(OH) 2 D 3 (100 nM, 24 h incubation). In diabetic animals, we found a significant reduction in the endothelial-dependent relaxation to acetylcholine and an increased expression of the MAO-A isoform, respectively. Vitamin D significantly improved vascular function, mitigated oxidative stress and decreased MAO-A expression in diabetic vascular preparations. In conclusion, MAO-A is induced in diabetic aortas and vitamin D can improve diabetes-induced endothelial dysfunction by modulating the MAO-A expression.

Published
2019
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5. Quercetin exerts an inhibitory effect on cellular bioenergetics of the B164A5 murine melanoma cell line.

Author

Sturza A, Pavel I, Ancușa S, Danciu C, Dehelean C, Duicu O, and Muntean D

Subjects
Animals, Cell Line, Tumor, Melanoma drug therapy, Melanoma pathology, Mice, Energy Metabolism drug effects, Melanoma metabolism, Oxygen Consumption drug effects, Quercetin pharmacology
Abstract

Modulation of mitochondrial bioenergetics and glycolysis in malignancies has recently emerged a potential chemotherapeutic strategy since numerous malignant cells have overcome inhibition of the glycolytic pathway by increasing mitochondrial ATP production. Quercetin is a flavonoid with antioxidant, antiangiogenic, and chemoprotective properties but the mitochondrial effects are less characterized. The present study was purported to assess the effects of quercetin on the bioenergetic profile of B164A5 murine melanoma cell line. The oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) were measured at 24, 48, and 72 h of treatment of B164A5 murine melanoma cells with increasing concentrations (25, 50, 100, and 150 µM) of quercetin using the extracellular flux analyzer Seahorse XF24e (Seahorse Agilent). Analysis of mitochondrial function was performed in the presence of the classic modulators of the electron transport chain: oligomycin, FCCP, and rotenone. 72-h treatment with quercetin induced a dose-dependent decrease of all OCR parameters (basal respiration, proton leak, ATP turnover, maximal respiration, reserve capacity) as well as of ECAR. At variance, 48-h treatment induced a decrease of OCR and ECAR when quercetin was applied at 50, 100, and 150 µM, while the 24-h treatment induced a decrease of bioenergetic parameters only for the highest concentrations (100 and 150 µM) of the compound. Our data clearly demonstrated that quercetin elicited dose-dependent inhibitory effect on examined parameters of cellular bioenergetics that was most potent at 72 h of treatment. Thereby quercetin, modulating both glycolytic and mitochondrial pathways for ATP production, might be an efficient approach in killing cancer cells.

Published
2018
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6. Monoamine oxidase inhibition improves vascular function and reduces oxidative stress in rats with lipopolysaccharide-induced inflammation.

Author

Rațiu C, Uțu D, Petruș A, Norbert P, Olariu S, Duicu O, Sturza A, and Muntean DM

Subjects
Animals, Hydrogen Peroxide, Inflammation, Lipopolysaccharides, Mice, Monoamine Oxidase, Monoamine Oxidase Inhibitors, Rats, Oxidative Stress
Abstract

Oxidative stress and vascular inflammation are the two major pathomechanisms that contribute to the progression of both cardiovascular and metabolic diseases. We have previously demonstrated that monoamine oxidases (MAOs), mitochondrial enzymes with two isoforms (A and B), are contributors to the endothelial dysfunction associated with inflammation in mice. The present study was purported to assess the effects of MAOs on endothelial dysfunction in rats with lipopolysaccharide (LPS)-induced acute inflammation. To this aim, aortas harvested from rats treated or not with a single dose of LPS were used for organ-bath studies of vascular reactivity and H2O2 production assessment in the presence vs. absence of MAO inhibitors. Our results demonstrate that MAO-A and B isoforms are induced in the rat vascular system after LPS administration. Both reversible and irreversible MAOs inhibition improved vascular function and reduced oxidative stress. In conclusion, MAOs are contributors to the occurrence of endothelial dysfunction in the rat model of LPS-induced acute inflammation. MAO inhibition may become a viable therapeutic strategy for the treatment of cardiometabolic disease.

Published
2018
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7. Activation of prosurvival signaling pathways during the memory phase of volatile anesthetic preconditioning in human myocardium: a pilot study.

Author

Mellidis K, Ordodi V, Galatou E, Săndesc D, Bubenek S, Duicu O, Muntean D, and Lazou A

Subjects
Aged, Anesthetics, General administration & dosage, Anesthetics, Inhalation pharmacology, Extracellular Signal-Regulated MAP Kinases metabolism, Female, Glycogen Synthase Kinase 3 metabolism, Glycogen Synthase Kinase 3 beta, Humans, Isoflurane pharmacology, Male, Methyl Ethers pharmacology, Middle Aged, Phosphorylation, Pilot Projects, Protein Kinase C-alpha metabolism, Protein Kinase C-delta metabolism, Proto-Oncogene Proteins c-akt metabolism, Sevoflurane, Signal Transduction drug effects, Thoracic Surgery, Anesthetics, General pharmacology, Heart drug effects, Ischemic Preconditioning, Myocardial methods, Myocardial Ischemia prevention & control
Abstract

According to a compelling body of evidence anesthetic preconditioning (APC) attenuates the deleterious consequences of ischemia-reperfusion and protects the heart through a mechanism similar to ischemic preconditioning. The present study was purported to investigate the intracellular signaling pathways activated in human myocardium in response to a preconditioning protocol with two different volatile anesthetics, namely isoflurane and sevoflurane. To this aim, phosphorylation of PKCα and -δ, ERK1/2, Akt, and GSK3β was determined at the end of the APC protocol, in human atrial samples harvested from patients undergoing open-heart surgery. The results demonstrate that preconditioning with volatile anesthetics triggers the activation of PKCδ and -α isoforms and of prosurvival kinases, ERK1/2, and Akt, while inhibiting their downstream target GSK3β during the memory phase.

Published
2014
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8. Betulinic acid as a potent and complex antitumor phytochemical: a minireview.

Author

Gheorgheosu D, Duicu O, Dehelean C, Soica C, and Muntean D

Subjects
Angiogenesis Inhibitors chemistry, Angiogenesis Inhibitors pharmacology, Angiogenesis Inhibitors therapeutic use, Animals, Antineoplastic Agents, Phytogenic chemistry, Antineoplastic Agents, Phytogenic pharmacology, Apoptosis drug effects, Humans, Neoplasm Metastasis, Neoplasms pathology, Pentacyclic Triterpenes, Phytochemicals chemistry, Phytochemicals pharmacology, Triterpenes chemistry, Triterpenes pharmacology, Betulinic Acid, Antineoplastic Agents, Phytogenic therapeutic use, Neoplasms drug therapy, Phytochemicals therapeutic use, Triterpenes therapeutic use
Abstract

Betulinic acid (BA), a natural compound with a lupan skeleton, has been highly investigated in the past decade for a plethora of beneficial properties, including anti-cancer, anti-inflammatory, anti-angiogenic, immune-modulatory, and anti-HIV effects. In particular, BA has been reported to be effective in vitro against tumor cell lines of different origins, and also in vivo, in animal models of cancer. The best characterized mechanism of its antitumor effect consists of triggering apoptosis via the mitochondrial pathway. BA has also an anti-metastatic effect via the prevention of the epithelial-to-mesencymal transition in highly aggressive melanoma cells. Furthermore, in the same model, BA is able to counteract the pro-invasive potential of the pro-tumoral protein neutrophil gelatinaseassociated lipocalin. The present review addresses the current state of knowledge regarding the anti-tumor effects of betulinic acid, a potent chemotherapeutic agent.

Published
2014
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9. Substrate-specific impairment of mitochondrial respiration in permeabilized fibers from patients with coronary heart disease versus valvular disease.

Author

Duicu O, Juşcă C, Falniţă L, Mirică S, Maximov D, Firă-Mladinescu O, and Muntean D

Subjects
Aged, Carbohydrate Metabolism, Cell Respiration, Coronary Artery Disease pathology, Electron Transport, Female, Glutamic Acid metabolism, Heart Valve Diseases pathology, Humans, In Vitro Techniques, Malates metabolism, Male, Middle Aged, Mitochondria, Heart drug effects, Oxidative Phosphorylation, Oxygen Consumption, Permeability, Saponins pharmacology, Coronary Artery Disease metabolism, Heart Valve Diseases metabolism, Mitochondria, Heart metabolism, Myocytes, Cardiac metabolism
Abstract

High-resolution respirometry of permeabilized myocardial fibers offers reliable insights concerning the integrated mitochondrial function while using small amounts of cardiac tissue. The aim of the present study was to assess the respiratory function in permeabilized fibers of human right atrial appendages harvested from patients with coronary heart disease (CHD) (n = 6) versus patients with valvular disease (n = 5) and preserved ejection fraction that underwent non-emergency cardiac surgery. Human bundle samples (1-3 mg wet weight) permeabilized with saponin were transferred into the 2 ml Oxygraph-2 k chambers to measure complex I(CI) and II (CII)-dependent respiration, respectively. The following values (expressed in pmol/s mg) were obtained for CI-dependent respiration: oxidative phosphorylation (OXPHOS), 35.65 ± 1.10 versus 42.43 ± 1.08, electron transport system (ETS), 37.87 ± 1.72 versus. 46.58 ± 1.85, and respiratory control ratio (RCR, calculated as the ratio between OXPHOS and LEAK states), 2.43 ± 0.09 versus 2.73 ± 0.068 (p < 0.05). In conclusion, in patients with CHD we showed a significant decline for the OXPHOS capacity, ETS and RCR for mitochondria energized with CI (but not with CII) substrates. These observations are suggestive for an early impairment of complex I supported respiration in ischemic heart disease, as previously demonstrated in the setting of experimental ischemia/reperfusion in several animal species.

Published
2013
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10. Monoamine oxidase--a inhibition reverses endothelial dysfunction in hypertensive rat aortic rings.

Author

Sturza A, Mirică SN, Duicu O, Gheorgheosu D, Noveanu L, Fira-Mlădinescu O, and Muntean DM

Subjects
Acetylcholine pharmacology, Animals, Endothelium, Vascular enzymology, Endothelium, Vascular physiopathology, Female, In Vitro Techniques, Models, Cardiovascular, Nitroprusside pharmacology, Oxidative Stress drug effects, Rats, Rats, Inbred SHR, Rats, Wistar, Vasodilator Agents pharmacology, Aorta drug effects, Clorgyline pharmacology, Endothelium, Vascular drug effects, Hypertension physiopathology, Monoamine Oxidase biosynthesis, Monoamine Oxidase Inhibitors pharmacology
Abstract

Aim: Monoamine oxidases (MAOs) are mitochondrial enzymes, with 2 isoforms, A and B that convert biogenic amines to their corresponding aldehydes via a reaction that produces hydrogen peroxide. Since MAO-A is the predominant form at vascular level we hypothesized that MAO-A-dependent H2O2 production may contribute to the development of endothelial dysfunction and, MAOs inhibition could improve the vascular function, respectively., Material and Methods: To this aim aortic rings were isolated from female adult spontaneously hypertensive rats (SHR) and their corresponding (Wistar-Kyoto) controls. The effect of MAO-A inhibitor, clorgyline (10 micromol/l) on endothelium-dependent relaxation (EDR) in response to acetylcholine and endothelium-independent relaxation in response to sodium nitroprusside, was studied in isolated phenylephrine-preconstricted aortic segments in the presence of indometacine (10 micromol/l)., Results: In hypertensive group EDR was significantly decreased - maximal relaxation (% of KCI, mean +/- SD) being 37 +/- 3.5 in SHR vs. 3.7 +/- 1.8 in controls. If experiments were done in the presence of clorgyline, EDR in control segments was unaffected. However, the compound restored normal EDR in aortic segments from hypertensive rats (maximal relaxation % of KCI, 13.7 +/- 2.3)., Conclusions: Inhibition of the MAO-A isoform might be useful in restoring endothelium-dependent relaxation in this experimental model of hypertension in rat.

Published
2013

11. Morphological and functional aspects of sciatic nerve regeneration after crush injury.

Author

Răducan A, Mirică S, Duicu O, Răducan S, Muntean D, Fira-Mlădinescu O, and Lighezan R

Subjects
Animals, Female, Myelin Sheath pathology, Rats, Rats, Sprague-Dawley, Sciatic Nerve injuries, Nerve Crush, Nerve Regeneration physiology, Recovery of Function physiology, Sciatic Nerve pathology, Sciatic Nerve physiopathology
Abstract

Experimental models for the investigation of nerve regeneration are critical in studying new strategies able to promote the repair process. The aim of the present work was to characterize morphological and functional aspects of sciatic nerve regeneration after mechanical crush injury in rodents. Morphological changes were assessed after a four minutes sciatic nerve injury induced by means of a standardized compression clip. Rat nerve samples were collected before injury and after 24 hours, four days, two weeks, and four weeks after injury, respectively. In an additional group with unilateral sciatic nerve injury, animals were evaluated for four weeks using walking track analysis and the sciatic static index (SSI) measured in both rearing and normal standing position. Histological study showed important axonal degeneration at four days and axonal regeneration at four weeks after injury. We observed no significant differences between SSI in rearing and normal standing stance and a strong correlation between SSI values measured in the two positions during the evaluation period. Positive correlations were also found for the footprint parameters. Our data provide a baseline characterization of the sciatic nerve crush injury that will further allow the investigation of peripheral nerve regeneration in the presence of potential neuroprotective agents in post-traumatic nerve repair.

Published
2013

12. High-resolution respirometry with multiple substrates titration in permeabilized myocardial fibers.

Author

Duicu O, Gheorgheosu D, Mirica N, Trancotă S, Cristina D, Firă-Mladinescu O, and Muntean D

Subjects
Algorithms, Animals, Male, Oxidative Coupling, Oxygen Consumption, Permeability, Rats, Saponins pharmacology, Titrimetry methods, Mitochondria, Heart metabolism, Myocytes, Cardiac metabolism, Oxidative Phosphorylation
Abstract

The present study was purported to standardize the high-resolution respirometry technique for the analysis of oxidative phosphorylation (OXPHOS) in saponin-skinned cardiac fibers. Preparation of permeabilized myocardial fibers allows the assessment of respiratory function of the entire population of mitochondria in their normal intracellular position. Adult male rat ventricular bundles were permeabilized with saponin (50 microg/ml) and samples (1-3 mg wet weight) were transferred into the Oxygraph-2k (OROBOROS Instr., Austria) chambers containing air saturated incubation buffer in order to measure Complex I (CI) and II (CII) dependent respiration. The following values (expressed in pmol O2 x s(-1) x mg(-1)) were obtained: CI&#95;LEAK, 67.18 +/- 5.12 (CI dependent basal respiration, after glutamate and malate addition); CI&#95;P, 247.37 +/- 49.90 (CI&#95;OXPHOS state after ADP addition); CI&#95;Pc, 252.036 +/- 53.13 (the intactness of the outer mitochondrial membrane assessed after cytochrome c addition); CI+II&#95;P, 342.90 +/- 62.48 (maximum OXPHOS state obtained after succinate addition by activating convergent electron flow from CI+II into the Q junction of the electron transport system (ETS); CII&#95;P, 302.26 +/- 50.16 (CII dependent OXPHOS state obtained after the addition of a CI inhibitor rotenone, with the subsequent entry of electrons from CII only into the Q junction); ETS capacity, 331.11 +/- 62.39 (uncoupled respiration). The standardized technique will allow the systematic characterization of mitochondrial respiratory dysfunction associated with several cardiac pathologies in both animals and humans.

Published
2012

13. The protective effect of superoxide dismutase on isolated human mammary arteries preincubated with triglyceride-rich remnant lipoproteins.

Author

Savoiu G, Drăgan S, Cristescu C, Serban C, Noveanu L, Ionescu D, Nicola T, Duicu O, Răducan A, and Voicu M

Subjects
Atherosclerosis drug therapy, Atherosclerosis physiopathology, Atherosclerosis prevention & control, Endothelium, Vascular physiopathology, Free Radical Scavengers pharmacology, Humans, In Vitro Techniques, Mammary Arteries drug effects, Superoxide Dismutase pharmacology, Endothelium, Vascular drug effects, Free Radical Scavengers metabolism, Lipoproteins adverse effects, Superoxide Dismutase metabolism, Triglycerides adverse effects, Vasodilation drug effects
Abstract

Unlabelled: The main changes of the plasma lipid profile in patients with endothelial dysfunction are the increased triglyceride content of the lipoprotein remnant particles, the presence of the small and dense LDL particles and the decreasing of the HDL-cholesterol level., Material and Method: Considering these observations, we performed "in vitro" experiments using human mammary artery rings, in order to examine the effect of the lipoprotein "remnants" on endothelium-dependent vasodilatation induced by cumulative doses (10(-9) M - 10(-4) M) of adenosine (ADP) and to study the effect on endothelial--independent vasodilatation induced by cumulative doses (10(-9) M-10(-4) M) of sodium-nitropruside (NSP), respectively., Results: Our results showed that 1 hour pre-incubation with triglyceride--rich lipoprotein remnants diminished the endothelial-dependent vasodilator response to ADP, but it has not modified the endothelial-independent vasodilator response to NSP. Vascular response was expressed as maximal vasodilatation from the 10(-4)M phenilephrine (PE) induced pre-contraction, considered as reference. In the case of ADP, the maximal vasodilatation was ranged in 36.50% +/- 10.81% interval, comparing with the control group that presented a maximal vasodilatation of 66.15% +/- 19.41% (p < 0.005). In the case of NSP the maximal vasodilatation was ranged in 99.78% +/- 10.53% interval, comparing with the control that presented a maximal vasodilatation of 98.99% +/- 12.45% (p = 0.44). One hour co-incubation of the rings with a solution containing lipoprotein remnants (1% oxidized IDL (ox-IDL) and antioxidant factor (150 U/mL 10(-4) M Superoxid dismutase (SOD) significantly reduced the impairment of the vasodilatation response to ADP. Maximal vasodilatation of ox-IDL and SOD coincubated human mammary artery rings was 58.50% +/- 10.63% compared to the control, were the maximal vasodilatation was 66.15% +/- 19.41% (p < 0.01), but has not modified the vasodilatation response to NSP (99% +/- 0.53% vs control 98.99% +/- 12.45%, p = 0.56)., Conclusion: The endothelial dysfunction induced by the triglyceride-rich lipoprotein "remnants", could contribute to the pathogenesis of atherosclerosis and the treatment with high doses of antioxidants could "protect" the endothelium against the pro-atherogenic action of the lipoprotein "remnants".

Published
2009

14. Measurement of plasma ox-LDL and carotid IMT may represent useful markers for atherosclerosis and may represent potential targets for therapeutic interventions.

Author

Savoiu G, Drăgan S, Cristescu C, Serban C, Noveanus L, Ionescu D, Nicola T, Duicu O, Raducan A, and Voicu M

Subjects
Aged, Algorithms, Biomarkers blood, Carotid Artery Diseases diagnostic imaging, Carotid Artery Diseases therapy, Carotid Artery, Common diagnostic imaging, Carotid Artery, Internal pathology, Cholesterol, HDL blood, Cholesterol, LDL blood, Female, Humans, Male, Middle Aged, Risk Factors, Statistics, Nonparametric, Triglycerides blood, Tunica Intima diagnostic imaging, Tunica Media diagnostic imaging, Ultrasonography, Carotid Artery Diseases blood, Carotid Artery Diseases pathology, Carotid Artery, Common pathology, Hypertension complications, Lipoproteins, LDL blood, Tunica Intima pathology, Tunica Media pathology
Abstract

Unlabelled: Oxidation of LDL plays an important role in the pathogenesis of atherosclerosis. Increased wall thickness precedes plaque formation and noninvasive B-mode ultrasonographic measurement of IMT is considered a useful marker of the development of the carotid atherosclerosis., Material and Method: The present study was designed to assess the association of oxidized low-density lipoprotein (ox-LDL) with carotid intima-media thickness (IMT) in hypertensive patients. Oxidized LDL (enzyme-linked immunosorbent assay, Elisa) and carotid IMT (high-resolution B-mode ultrasonography) were assessed in 74 patients, aged between 45 and 65 years, diagnosticated with arterial hypertension., Results: We observed significantly higher plasma levels of total cholesterol (236.32 +/- 41.96 mg/dl), LDL cholesterol (166.92 +/- 38.55 mg/dl), triglycerides (180.79 +/- 72.05 mg/dl) and low plasma levels of HDL-cholesterol (33.24 +/- 7.99 mg/dl) in all patients. We noticed higher plasma levels of ox-LDL (77.34 +/- 24.78 mg/dl) and carotid IMT was increased (1.41 +/- 0.31 mm). The statistically analysis done using Pearson's test and Student's t - test indicated that there were correlations of ox-LDL with: IMT (p < 0.05, r = 0.408), total cholesterol (p < 0.05, r = 0.498), LDL-cholesterol (p < 0.05, r = 0.527), triglycerides (p < 0.05, r = 0.385) and HDL-cholesterol (p < 0.05, r = -0.442)., Conclusion: Higher plasma levels of ox-LDL were associated with increased carotid IMT in hypertensive patients. Measurement of plasma Ox-LDL and carotid IMT may represent useful markers for atherosclerosis and may represent potential targets for therapeutic interventions.

Published
2009

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