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1. Aldosterone and Its Blockade: A Cardiovascular and Renal Perspective

Author

V. Lahera, V. Cachofeiro, G. Balfagon, and J.L. Rodicio

Subjects
Technology, Medicine, Science
Abstract

Aldosterone not only contributes to salt and water homeostasis, but also exerts direct cardiovascular and renal effects. Numerous experimental and clinical studies indicate that aldosterone participate in cardiac alterations associated with hypertension, heart failure, diabetes and other pathological entities. It is important to mention that dietary salt is a key factor in aldosterone-mediated cardiovascular damage, since damage was moreevident in animals on a high-salt diet than animals on a low salt diet. A pathophysiological action of aldosterone involves development of extracellular matrix and fibrosis, inflammation, stimulation of reactive oxygen species production, endothelial dysfunction, cell growth and proliferation. Many studies showed local extra-adrenal production of aldosterone in brain blood vessel, and the heart, which contribute in an important manner to the pathological actions of this mineralocorticoid.Several studies such as RALES, EPHESUS, 4E and others, recently showed that mineralocorticoid-receptor (MR) antagonists, alone or in combination with ACE inhibitors or ARBs, reduced the risk of progressive target organ damage and hospitalization in patients with hypertension and heart failure. These clinical benefits support the therapeutic usefulness of MR antagonists.

Published
2006
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3. Microsomal Prostaglandin E Synthase-1 (mPGES-1) plays a key role in the development of renal, metabolic and cardiovascular alterations associated with obesity

Author

C Ballesteros-Martinez, AM Briones, E Martínez-Martínez, María González-Amor, M Salaices, R Rodrigues-Diez, Luis M. Beltrán, and V Cachofeiro

Subjects
medicine.medical_specialty, Endocrinology, business.industry, Internal medicine, medicine, Microsomal Prostaglandin E Synthase-1, medicine.disease, business, Obesity
Published
2021

4. 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

5. Role of COX-2-derived PGE2on vascular stiffness and function in hypertension

Author

Mercedes Salaices, Dalton Valentim Vassallo, Luis Vila, J García-Puig, Roberto Palacios, María González-Amor, M V Cachofeiro, Ana M. Briones, María J. Alonso, Maylla Ronacher Simões, Luis M. Beltrán, María S. Avendaño, Sonia Martínez-Revelles, P Guillem-Llobat, and Andrea Aguado

Subjects
0301 basic medicine, Pharmacology, medicine.medical_specialty, Vascular smooth muscle, business.industry, Connective tissue, Inflammation, 030204 cardiovascular system & hematology, medicine.disease, Angiotensin II, Vascular remodelling in the embryo, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Endocrinology, medicine.anatomical_structure, Internal medicine, medicine, lipids (amino acids, peptides, and proteins), Endothelial dysfunction, medicine.symptom, business, Receptor, Vascular tissue
Abstract

Background and purpose Prostanoids derived from COX-2 and EP receptors are involved in vascular remodelling in different cardiovascular pathologies. This study evaluates the contribution of COX-2 and EP1 receptors to vascular remodelling and function in hypertension. Experimental approach Spontaneously hypertensive rats (SHR) and angiotensin II (AngII)-infused (1.44 mg · kg(-1) · day(-1), 2 weeks) mice were treated with the COX-2 inhibitor celecoxib (25 mg · kg(-1) · day(-1) i.p) or with the EP1 receptor antagonist SC19220 (10 mg · kg(-1) · day(-1) i.p.). COX-2(-/-) mice with or without AngII infusion were also used. Key results Celecoxib and SC19220 treatment did not modify the altered lumen diameter and wall : lumen ratio in mesenteric resistance arteries from SHR-infused and/or AngII-infused animals. However, both treatments and COX-2 deficiency decreased the augmented vascular stiffness in vessels from hypertensive animals. This was accompanied by diminished vascular collagen deposition, normalization of altered elastin structure and decreased connective tissue growth factor and plasminogen activator inhibitor-1 gene expression. COX-2 deficiency and SC19220 treatment diminished the increased vasoconstrictor responses and endothelial dysfunction induced by AngII infusion. Hypertensive animals showed increased mPGES-1 expression and PGE2 production in vascular tissue, normalized by celecoxib. Celecoxib treatment also decreased AngII-induced macrophage infiltration and TNF-α expression. Macrophage conditioned media (MCM) increased COX-2 and collagen type I expression in vascular smooth muscle cells; the latter was reduced by celecoxib treatment. Conclusions and implications COX-2 and EP1 receptors participate in the increased extracellular matrix deposition and vascular stiffness, the impaired vascular function and inflammation in hypertension. Targeting PGE2 receptors might have benefits in hypertension-associated vascular damage.

Published
2016

6. 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

7. 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

8. P143Mechanisms involved in the crosstalk between leptin and mineralocorticoid receptor in the cardiac fibrosis associated with obesity

Author

Natalia López-Andrés, M Miana, María Luisa Nieto, J. A. San Roman, Raquel Jurado-López, Ernesto Martínez-Martínez, V. Cachofeiro Ramos, Isabel Gallardo, Gema Marín-Royo, and Josué Gutiérrez-Tenorio

Subjects
medicine.medical_specialty, Physiology, Cardiac fibrosis, business.industry, Leptin, medicine.disease, Obesity, Crosstalk (biology), Mineralocorticoid receptor, Endocrinology, Physiology (medical), Internal medicine, medicine, Cardiology and Cardiovascular Medicine, business
Published
2018

9. Inflamación, disfunción endotelial e hipertensión arterial

Author

V. Lahera Juliá, N. de las Heras Jiménez, E. Cediel Gil, V. Cachofeiro Ramos, David Sanz-Rosa, and M. Miana Ortega

Subjects
Internal Medicine, Cardiology and Cardiovascular Medicine
Abstract

El proceso inflamatorio agudo y cronico determinan cambios importantes en los componentes de la sangre, tanto celulares como los no celulares, incluidos proteinas, lipidos, hormonas, citocinas, asi como otras moleculas. Algunos de estos marcadores de inflamacion como las citocinas, y especialmente la proteina C reactiva (PCR), se consideran en la actualidad predictores de eventos cardiovasculares. Ademas, la PCR favorece el desarrollo de la disfuncion endotelial al reducir la produccion de oxido nitrico (NO), sugiriendo, por tanto, un papel de la inflamacion en el desarrollo de las alteraciones de la funcion endotelial. Asimismo existen datos que indican que la disfuncion endotelial favorece el desarrollo inflamatorio. Una relacion compleja tambien se ha observado entre inflamacion e hipertension arterial; niveles elevados de presion arterial se asocian con un incremento de los niveles plasmaticos de algunos marcadores de inflamacion y, a su vez, una elevacion de los marcadores de inflamacion parecen predecir el riesgo de desarrollar hipertension.

Published
2004

11. Hipercolesterolemia y disfunción endotelial: mecanismos implicados

Author

N. de las Heras Jiménez, V. Lahera Juliá, E. Cediel Gil, V. Cachofeiro Ramos, E. Olivares, S. Vázquez-Pérez, and David Sanz-Rosa

Subjects
Internal Medicine, Cardiology and Cardiovascular Medicine
Abstract

El endotelio desempena un papel clave en la regulacion de la funcion vascular al liberar, en respuesta a distintos estimulos, numerosos factores vasoactivos. La hiperlipidemia, asi como otros factores de riesgo cardiovascular, alteran ese papel homeostatico que desempena el endotelio en la regulacion de la funcion vascular. Uno de los mecanismos fundamentales que subyacen a la disfuncion endotelial parece ser una disminucion en la disponibilidad de oxido nitrico (NO), lo que permite la sobreexpresion de las acciones de factores que se oponen a los efectos beneficiosos y protectores de este sobre la pared vascular. Diversos mecanismos podrian ser responsables de esta menor disponibilidad de NO, desde alteraciones en su sintesis a una mayor degradacion como consecuencia de un aumento del estres oxidativo. En pacientes hipercolesterolemicos la reduccion de los niveles de colesterol conlleva una mejoria de la funcion endotelial, lo que indicaria que la elevacion de dichos niveles podria activar diversos mecanismos que alteraran el normal funcionamiento del endotelio. Sin embargo, existen otros grupos de farmacos, como los antioxidantes o los que bloquean el sistema renina-angiotensina, que han demostrado un efecto beneficioso sobre la funcion endotelial tanto en estudios clinicos como experimentales.

Published
2003

12. Role of endothelin-1 and thromboxane A2 in renal vasoconstriction induced by angiotensin II in diabetes and hypertension

Author

D. Sanz-Rosa, V. Cachofeiro, Natalia De Las Heras, Vicente Lahera, Eva Cediel, Josefa Navarro-Cid, and Beatriz Vázquez-Cruz

Subjects
Endothelin Receptor Antagonists, Male, medicine.medical_specialty, kidney, hypertension, chronic renal disease, Blood Pressure, Rats, Inbred WKY, Receptors, Thromboxane A2, Prostaglandin H2, Diabetes Mellitus, Experimental, Renal Circulation, Thromboxane A2, chemistry.chemical_compound, Internal medicine, Rats, Inbred SHR, Medicine, Animals, Oxazoles, renal vascular resistance, Kidney, Angiotensin II receptor type 1, Dose-Response Relationship, Drug, Endothelin-1, diabetes, business.industry, Receptors, Endothelin, Angiotensin II, Bridged Bicyclo Compounds, Heterocyclic, Endothelin 1, Rats, medicine.anatomical_structure, Endocrinology, Losartan, Blood pressure, chemistry, Vasoconstriction, Nephrology, cardiovascular system, Vascular Resistance, medicine.symptom, arterial pressure, business, Oligopeptides, medicine.drug, circulatory and respiratory physiology
Abstract

Role of endothelin-1 and thromboxane A2 in renal vasoconstric- through a variety of mechanisms [1–3]. In addition, thromtion induced by angiotensin II in diabetes and hypertension. boxane A2 (TXA2) and endothelin-1 (ET-1) exert vascuBackground. Interactions among angiotensin II (Ang II), lar renal and systemic actions similar to those of Ang II, endothelin-1 (ET-1) and thromboxane A2 (TXA2) may play and may play a role in the renal alterations associated an important role in the regulation of renal function. The preswith hypertension and diabetes [4–6]. Altered vascular ent study investigated the participation of TXA2 and ET-1 in the increase in renal vascular resistances (RVR) induced by reactivity as well as increased production of different Ang II, as well as the consequences of diabetes, hypertension, vasoconstrictors including serotonin, noradrenalin, Ang II, and the combination of both on this response. ET-1 and TXA2, have been reported in experimental Methods. Isolated kidneys from male normoglycemic or models of diabetes and hypertension, yielding a variety streptozotocin-induced diabetic Wistar-Kyoto rats (WKY) and of results [4–9]. Several studies reported interactions spontaneously hypertensive rats (SHR) were used. The increase in perfusion pressure (PP) produced by Ang II was studied among Ang II, ET-1 and TXA2 that could be important in in the absence or presence of the TXA2 receptor antagonist, the regulation of renal function [7, 9–11]. We previously ifetroban, or the ETA/ETB receptor antagonist, PD145065. observed that the angiotensin II type 1 (AT1) receptor Results. Systolic arterial pressure (SAP) was higher in SHR antagonist losartan reduced constrictor responses to ET-1 than in WKY, but diabetic rats (D) from each strain showed and a TXA 2 analog in aortic rings from spontaneously lower SAP values than their respective non-diabetic rats. Basal

Published
2002
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13. AT 1 Receptor Antagonism Reduces Endothelial Dysfunction and Intimal Thickening in Atherosclerotic Rabbits

Author

Josefa Navarro-Cid, V. Cachofeiro, M. Degasparo, Rosaura Maeso, Paloma Aragoncillo, J. Mann, N. de las Heras, Luis M. Ruilope, Vicente Lahera, and S. Vázquez-Pérez

Subjects
Male, medicine.medical_specialty, Endothelium, Arteriosclerosis, Tetrazoles, Angiotensin Receptor Antagonists, chemistry.chemical_compound, Internal medicine, Renin–angiotensin system, Internal Medicine, medicine, Animals, Endothelial dysfunction, Receptor, Antihypertensive Agents, Aorta, Receptors, Angiotensin, Angiotensin II receptor type 1, business.industry, Cholesterol, Valine, medicine.disease, Angiotensin II, Endocrinology, medicine.anatomical_structure, Valsartan, chemistry, Endothelium, Vascular, Rabbits, Angiotensin I, Tunica Intima, business, medicine.drug
Abstract

Abstract —The effects of angiotensin (AT) 1 receptor antagonists on functional and morphological alterations associated with atherosclerosis are not well known. The current study was performed to examine the long-term effects of valsartan (3 or 10 mg/kg per day for 10 weeks) on endothelial function and structural changes in aorta from rabbits fed with either a control diet or a cholesterol-enriched diet. Rabbits fed with the cholesterol-rich diet showed higher ( P P P P 1 receptors, appears to play a key role in the development of the vascular functional and structural changes associated with hypercholesterolemia. AT 1 receptor antagonists, besides their antihypertensive effects, could be an important therapeutic tool to reduce the development of atherosclerosis.

Published
1999

14. Role of thromboxane, catecholamines and endothelin-1 in the renal constrictor response to angiotensin II in diabetic hypertensive rats

Author

B, Vázquez-Cruz, E, Cediel, V, Cachofeiro-Ramos, and V, Lahera-Julia

Subjects
Blood Glucose, Male, Hypertension, Renal, Endothelin-1, Angiotensin II, Body Weight, Thromboxanes, Blood Pressure, In Vitro Techniques, Rats, Inbred WKY, Diabetes Mellitus, Experimental, Rats, Renal Circulation, Catecholamines, Rats, Inbred SHR, Animals, Vasoconstrictor Agents
Published
2002

15. In vivo tissue specific modulation of rat insulin receptor gene expression in an experimental model of mineralocorticoid excess

Author

J, Campión, V, Lahera, V, Cachofeiro, B, Maestro, N, Dávila, M C, Carranza, and C, Calle

Subjects
Epididymis, Male, Receptor, Insulin, Hindlimb, Rats, Disease Models, Animal, Adipose Tissue, Gene Expression Regulation, Liver, Organ Specificity, Mineralocorticoids, Hyperaldosteronism, Animals, Humans, Insulin, RNA, Messenger, Rats, Wistar, Desoxycorticosterone, Muscle, Skeletal
Abstract

Insulin receptor (IR) gene expression at the mRNA level was investigated in hindlimb skeletal muscle, epididymal adipose tissue and in the liver of rats exposed to prolonged in vivo administration of deoxycorticosterone acetate (DOCA). Following treatment, plasma insulin levels were reduced while glucose levels increased compared to values in control rats. DOCA-treated animals showed an increase in blood pressure and a reduction in body weight. This treatment also induced hypokalemia and decreased plasma protein levels. Sodium levels were unaffected. Moreover, no differences in DNA and protein content or in the indicator of cell size (protein/DNA) were observed in the skeletal muscle or adipose tissue of animals. In contrast, there was a clear increase in the protein and DNA contents of the liver with no change in the indicator of cell size. Northern blot assays revealed 2 major IR mRNA species of approximately 9.5 and 7.5 Kb in the 3 tissues from control animals. DOCA treatment induced no change in the levels of either RNA species in skeletal muscle. However, a decrease of approximately 22% was detected in the levels of both species in adipose tissue whereas the liver showed an increase of 64%. These results provide the first evidence for an in vivo tissue-specific modulation of IR mRNA levels under experimental conditions of mineralocorticoid excess.

Published
1998

16. GALECTIN-3 IS A POTENTIAL MEDIATOR OF ALDOSTERONE EFFECTS IN VASCULAR REMODELING

Author

Laurent Calvier, Beatriz Martín-Fernández, Faiez Zannad, Natalia López-Andrés, P. Lacolley, Patrick Rossignol, V. Lahera, and V. Cachofeiro

Subjects
chemistry.chemical_compound, Aldosterone, Mediator, chemistry, Physiology, Galectin-3, business.industry, Internal Medicine, Cancer research, Medicine, Cardiology and Cardiovascular Medicine, business
Published
2011

18. P0507 DIFFERENT ALCOHOLIC BEBERAGES INFLUENCE IN ANTIOXIDANT PLASMA CAPACITY

Author

Eduardo Oliveros Acebes, Robeto Salomon Perez, V Lahera, Diana Salor Moral, Jesus Millan Nuñez-Cortes, Olga Marin Casajus, Maria Ferrer Civeira, Carlos Recarte, Encarnacion Vilalta Castel, and V Cachofeiro

Subjects
Antioxidant, business.industry, medicine.medical_treatment, Internal Medicine, medicine, Food science, business
Published
2009

19. Consequences of aldosterone administration on cardiac ion currents in rats

Author

Sandra Ballesteros, Carmen Delgado, V. Lahera, B. Marin‐Fernandez, N. de las Heras, María Miana, and V. Cachofeiro

Subjects
medicine.medical_specialty, chemistry.chemical_compound, Endocrinology, Aldosterone, chemistry, business.industry, Internal medicine, Medicine, Pharmacology, Cardiology and Cardiovascular Medicine, business, Administration (government)
Published
2008

20. ROLE OF ALDOSTERONE ON VASCULAR ALTERATIONS ASSOCIATED WITH HYPERTENSION IN RATS

Author

K. Giuberti, T. Fernandes, V. Cachofeiro, V. Lahera, F.M. Pecanha, D. Sanz-Rosa, N. de las Heras, María Miana, and Beatriz Martín

Subjects
Vascular Alterations, medicine.medical_specialty, Aldosterone, business.industry, General Medicine, medicine.disease, chemistry.chemical_compound, Endocrinology, chemistry, Pathophysiology of hypertension, Internal medicine, Internal Medicine, Medicine, Cardiology and Cardiovascular Medicine, business
Published
2008

23. PARTICIPATION OF ALDOSTERONE IN THE OXIDATIVE STRESS ASSOCIATED WITH HYPERTENSION

Author

V. Cachofeiro, María Miana, E. Cediel, D. Sanz-Rosa, V. Lahera, Pilar Oubiña, and N. de las Heras

Subjects
medicine.medical_specialty, Aldosterone, Physiology, business.industry, medicine.disease_cause, medicine.disease, chemistry.chemical_compound, Endocrinology, chemistry, Internal medicine, Pathophysiology of hypertension, Internal Medicine, medicine, Cardiology and Cardiovascular Medicine, business, Oxidative stress
Published
2004

25. W01.47 Effect of atorvastatin and gemfibrozil on inflammatory markers in dyslipidemic patients with and without coronary artery disease

Author

V. Lahera, P.L. pez Jaramillo, Juan P. Casas, M. P. Oubina, Federico Silva, L. A. Cubillos, and V. Cachofeiro

Subjects
medicine.medical_specialty, business.industry, Atorvastatin, General Medicine, medicine.disease, Coronary artery disease, Internal medicine, Internal Medicine, Cardiology, Medicine, Gemfibrozil, Cardiology and Cardiovascular Medicine, business, medicine.drug
Published
2004

26. W01.75 Angiotensin II receptor antagonism ameliorates endothelial dysfunction and reduces inflammation in hypertensive rats

Author

V. Lahera, V. Cachofeiro, María Miana, E. Cediel, N. de las Heras, and D. Sanz-Rosa

Subjects
Angiotensin receptor, Angiotensin II receptor type 1, biology, business.industry, Inflammation, Angiotensin-converting enzyme, General Medicine, Pharmacology, medicine.disease, Internal Medicine, medicine, biology.protein, medicine.symptom, Endothelial dysfunction, Cardiology and Cardiovascular Medicine, business, Antagonism
Published
2004

29. The impact of hypertriglyceridemia on endothelial function, vascular structure and fibrinolysis in hypercholesterolemic rabbits

Author

Luis M. Ruilope, V. Lahera, Beatriz Vázquez-Cruz, S. Vázquez-Pérez, V. Cachofeiro, N. de las Heras, D. Sanz-Rosa, Paloma Aragoncillo, E. Cediel, and M. P. Oubina

Subjects
medicine.medical_specialty, business.industry, medicine.medical_treatment, Hypertriglyceridemia, General Medicine, medicine.disease, Endocrinology, Internal medicine, Fibrinolysis, Internal Medicine, medicine, Vascular structure, Cardiology and Cardiovascular Medicine, business, Function (biology)
Published
2001

30. Atorvastatin prevents glomerulosclerosis and renal endothelial dysfunction in atherosclerotic rabbits

Author

C. Diaz, Paloma Aragoncillo, E. Cediel, Gonzalo Hernández, N. de las Heras, D. Sanz-Rosa, V. Cachofeiro, S. Vázquez-Pérez, V. Lahera, Luis M. Ruilope, and Beatriz Vázquez-Cruz

Subjects
medicine.medical_specialty, business.industry, Atorvastatin, Internal Medicine, Urology, Medicine, Glomerulosclerosis, General Medicine, Endothelial dysfunction, Cardiology and Cardiovascular Medicine, business, medicine.disease, medicine.drug
Published
2001

32. FACTORS INVOLVED IN ENDOTHELIUM-DEPENDENT RELAXATION IN CORONARY ARTERIES FROM HYPERTENSIVE RATS

Author

E. Cediel, L. Sloesen, Luis M. Ruilope, N. de las Heras, D. Sanz-Rosa, Josefa Navarro-Cid, V. Cachofeiro, V. Lahera, and S. Vázquez-Pérez

Subjects
Coronary arteries, medicine.medical_specialty, medicine.anatomical_structure, Physiology, business.industry, Internal medicine, Internal Medicine, Cardiology, medicine, Relaxation (physics), Endothelium dependent, Cardiology and Cardiovascular Medicine, business
Published
2000

33. ROLE OF THROMBOXANE A2 AND CATECHOLAMINES ON THE RENAL RESPONSE TO ANGIOTENSIN II IN HYPERTENSIVE AND DIABETIC RATS

Author

Luis M. Ruilope, D. Sanz-Rosa, V. Cachofeiro, Josefa Navarro-Cid, N. de las Heras, V. Lahera, S. Vázquez-Pérez, L. Sloesen, and E. Cediel

Subjects
medicine.medical_specialty, Angiotensin receptor, Angiotensin II receptor type 1, Physiology, business.industry, Angiotensin II, Thromboxane A2, chemistry.chemical_compound, Endocrinology, chemistry, Internal medicine, Internal Medicine, medicine, Renal response, Cardiology and Cardiovascular Medicine, business
Published
2000

35. Glomerular and vascular atrial natriuretic factor receptors in adrenalectomized rats

Author

V. Cachofeiro, Ernesto L. Schiffrin, Marc Cantin, and Raul Garcia

Subjects
Male, medicine.medical_specialty, Kidney Cortex, Physiology, Renal glomerulus, medicine.medical_treatment, Kidney Glomerulus, Blood Pressure, Receptors, Cell Surface, Dexamethasone, Muscle, Smooth, Vascular, Atrial natriuretic peptide, Furosemide, Reference Values, Physiology (medical), Internal medicine, Renin, otorhinolaryngologic diseases, medicine, Animals, Desoxycorticosterone, Receptor, Aorta, Kidney, business.industry, Myocardium, Adrenalectomy, Rats, Inbred Strains, musculoskeletal system, Mesenteric Arteries, Rats, medicine.anatomical_structure, Endocrinology, Hematocrit, embryonic structures, Circulatory system, cardiovascular system, business, Receptors, Atrial Natriuretic Factor, Atrial Natriuretic Factor, hormones, hormone substitutes, and hormone antagonists, medicine.drug, Blood vessel
Abstract

The renal and vascular responses to atrial natriuretic factor (ANF) and glomerular and vascular ANF receptors were studied in adrenalectomized (ADR) rats with or without deoxycorticosterone (DOC) or dexamethasone (Dexa) replacement therapy. As expected, adrenalectomy elicited hypotension, hemoconcentration, and increased plasma renin activity, but no changes in plasma levels of either ANF-(1-98) or ANF-(99-126) were detected. Dexa treatment decreased both ANF-(1-98) and ANF-(99-126), whereas DOC treatment increased only ANF-(1-98). The acute renal response to ANF and furosemide was reduced in ADR rats and partially restored either by steroid replacement or by raising blood pressure. The blunted natriuretic response to ANF in ADR rats was associated with an increased density of glomerular receptors. Norepinephrine-precontracted vascular strips from ADR rats were more sensitive to ANF (ED50: 1.7 x 10(-8) M) than those from sham-operated animals (ED50: 1.5 x 10(-7) M). However, vascular ANF receptor density in mesenteric vessels from ADR animals was decreased. Dexa treatment restored vascular response to that observed in sham-operated animals without a concomitant change in vascular receptor density. Because the presence of guanylate cyclase-coupled and noncoupled ANF receptor subtypes have been described in different tissues, we conclude that the apparent lack of correlation between the biological response to ANF and total binding of ANF to glomeruli or mesenteric artery membranes in ADR rats may be in part caused by a differential regulation of both receptor subtype populations.

Published
1989

36. Acute effect of potassium canrenoate administration on renin-angiotensin, kallikrein-kinin and prostaglandin systems

Author

V, Lahera, V, Cachofeiro, F, Duran, F J, Cañizo, F J, Rodriguez, and J A, Tresguerres

Subjects
Male, Body Weight, Sodium, Blood Pressure, Rats, Inbred Strains, Sodium, Dietary, Kinins, Diet, Diuresis, Rats, Renin-Angiotensin System, Pregnadienes, Renin, Potassium, Prostaglandins, Animals, Kallikreins, Canrenoic Acid, Injections, Intraperitoneal
Abstract

1. To investigate the possible effects of potassium canrenoate (PC) on plasma renin activity (PRA) and on renal prostaglandins (PGS) and kinins under elevated sodium and/or potassium intakes, a single dose of PC was administered to four groups of Wistar male rats. 2. They were fed a normal diet (C), a diet supplemented with 4% of NaCl, (Na), with 1% of KCl: (K) or both supplements (NaK). 3. PRA and urinary PGS excretion did not show changes after PC administration, but total urinary kinins showed higher values after the treatment in all groups. 4. A diuretic but not natriuretic effect was observed only in C animals. 5. In conclusion, the single dose of PC was able to stimulate urinary kinins and to spare potassium independently of dietary electrolyte supplements that were able to block the diuretic effect of the drug.

Published
1988

39. Effect of potassium canrenoate on kinins and renin in rats

Author

F. Durán, J.J Cantón, F.J. Rodriguez, V Lahera, V Cachofeiro, and F.J. Cañizo

Subjects
medicine.medical_specialty, Endocrinology, Chemistry, Potassium canrenoate, Internal medicine, Renin–angiotensin system, medicine, Biochemistry, medicine.drug
Published
1986

40. The detrimental role of galectin-3 and endoplasmic reticulum stress in the cardiac consequences of myocardial ischemia in the context of obesity.

Author

Jiménez-González S, Delgado-Valero B, Islas F, Romero-Miranda A, Luaces M, Ramchandani B, Cuesta-Corral M, Montoro-Garrido A, Martínez-Martínez E, and Cachofeiro V

Subjects
Animals, Male, Rats, Humans, Pectins pharmacology, Middle Aged, Myocardial Infarction metabolism, Myocardial Infarction pathology, Myocardial Infarction complications, Female, Fibrosis, Rats, Wistar, Myocardial Ischemia metabolism, Myocardial Ischemia pathology, Phenylbutyrates pharmacology, Autophagy, Myocardium metabolism, Myocardium pathology, Galectins metabolism, Aged, Blood Proteins metabolism, Endoplasmic Reticulum Stress, Galectin 3 metabolism, Obesity metabolism, Obesity complications
Abstract

The association between cardiac fibrosis and galectin-3 was evaluated in patients with acute myocardial infarction (MI). The role of galectin-3 and its association with endoplasmic reticulum (ER) stress activation in the progression of cardiovascular fibrosis was also evaluated in obese-infarcted rats. The inhibitor of galectin-3 activity, modified citrus pectin (MCP; 100 mg/kg/day), and the inhibitor of the ER stress activation, 4-phenylbutyric acid (4-PBA; 500 mg/kg/day), were administered for 4 weeks after MI in obese rats. Overweight-obese patients who suffered a first MI showed higher circulating galectin-3 levels, higher extracellular volume, and LV infarcted size, as well as lower E/e'ratio and LVEF compared with normal-weight patients. A correlation was observed between galectin-3 levels and extracellular volume. Obese-infarcted animals presented cardiac hypertrophy and reduction in LVEF, and E/A ratio as compared with control animals. They also showed an increase in galectin-3 gene expression, as well as cardiac fibrosis and reduced autophagic flux. These alterations were associated with ER stress activation characterized by enhanced cardiac levels of binding immunoglobulin protein, which were correlated with those of galectin-3. Both MCP and 4-PBA not only reduced cardiac fibrosis, oxidative stress, galectin-3 levels, and ER stress activation, but also prevented cardiac functional alterations and ameliorated autophagic flux. These results show the relevant role of galectin-3 in the development of diffuse fibrosis associated with MI in the context of obesity in both the animal model and patients. Galectin-3 in tandem with ER stress activation could modulate different downstream mechanisms, including inflammation, oxidative stress, and autophagy., (© 2024 The Author(s). The FASEB Journal published by Wiley Periodicals LLC on behalf of Federation of American Societies for Experimental Biology.)

Published
2024
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41. Resolvin D2 prevents vascular remodeling, hypercontractility and endothelial dysfunction in obese hypertensive mice through modulation of vascular and proinflammatory factors.

Author

Rodrigues-Diez R, Ballesteros-Martinez C, Moreno-Carriles RM, Nistal F, Díaz Del Campo LS, Cachofeiro V, Dalli J, García-Redondo AB, Redondo JM, Salaices M, and Briones AM

Subjects
Animals, Male, Humans, Mice, Endothelium, Vascular drug effects, Endothelium, Vascular metabolism, Endothelium, Vascular pathology, Diet, High-Fat adverse effects, Angiotensin II, Aortic Aneurysm, Abdominal pathology, Aortic Aneurysm, Abdominal metabolism, Aortic Aneurysm, Abdominal drug therapy, Inflammation Mediators metabolism, Mice, Obese, Vasoconstriction drug effects, Inflammation pathology, Inflammation metabolism, Macrophages drug effects, Macrophages metabolism, Disease Models, Animal, Docosahexaenoic Acids pharmacology, Hypertension metabolism, Hypertension drug therapy, Mice, Inbred C57BL, Obesity complications, Obesity metabolism, Vascular Remodeling drug effects
Abstract

During resolution of inflammation, specialized proresolving mediators (SPMs), including resolvins, are produced to restore tissue homeostasis. We hypothesized that there might be a dysregulation of SPMs pathways in pathological vascular remodeling and that resolvin D2 (RvD2) might prevent vascular remodeling and contractile and endothelial dysfunction in a model of obesity and hypertension. In aortic samples of patients with or without abdominal aortic aneurysms (AAA), we evaluated gene expression of enzymes involved in SPMs synthesis (ALOXs), SPMs receptors and pro-inflammatory genes. In an experimental model of aortic dilation induced by high fat diet (HFD, 60%, eighteen weeks) and angiotensin II (AngII) infusion (four weeks), we studied the effect of RvD2 administration in aorta and small mesenteric arteries structure and function and markers of inflammation. In human macrophages we evaluated the effects of AngII and RvD2 in macrophages function and SPMs profile. In patients, we found positive correlations between AAA and obesity, and between AAA and expression of ALOX15, RvD2 receptor GPR18, and pro-inflammatory genes. There was an inverse correlation between the expression of aortic ALOX15 and AAA growth rate. In the mice model, RvD2 partially prevented the HFD plus AngII-induced obesity and adipose tissue inflammation, hypertension, aortic and mesenteric arteries remodeling, hypercontratility and endothelial dysfunction, and the expression of vascular proinflammatory markers and cell apoptosis. In human macrophages, RvD2 prevented AngII-induced impaired efferocytosis and switched SPMs profile. RvD2 might represent a novel protective strategy in preventing vascular damage associated to hypertension and obesity likely through effects in vascular and immune cells., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Published
2024
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42. Methodology for the induction of myocardial infarction and cardiac function evaluation.

Author

Islas F, Ramchandani B, Cuesta-Corral M, Montoro-Garrido A, Romero-Miranda A, Luaces M, Martínez-Martínez E, and Cachofeiro V

Subjects
Rats, Humans, Animals, Disease Models, Animal, Myocardium, Heart, Ventricular Function, Left, Myocardial Infarction diagnostic imaging
Abstract

Cardiovascular disease (CVD) is the main cause of death worldwide, with myocardial infarction (MI) being the most prevalent pathology involved in CVD. MI is characterized by a deficiency in oxygen supply to the myocardium, thereby promoting ventricular remodeling of the ischemic and remote zone of the heart. Cardiac remodeling associated with MI could promote the development of heart failure and finally death. For these reasons, it is important to develop animal models that mimic human cardiac disease which could help to identify new mechanisms involved in the pathology and, consequently, develop new therapeutic strategies. We herein describe in detail a protocol for MI induction with low mortality rate (<15%) in rats by ligation of the left anterior descending artery. In addition, we also describe two imaging techniques which allow to evaluate cardiac structure and function-including deformation parameters in rats such as transthoracic echocardiography and cardiac magnetic resonance. This animal model could be useful for acute and chronic studies and for evaluating the potential usefulness of different treatments., (Copyright © 2024 Elsevier Inc. All rights are reserved, including those for text and data mining, AI training and similar technologies.)

Published
2024
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43. Importance of cardiac imaging assessment of epicardial adipose tissue after a first episode of myocardial infarction.

Author

Islas F, Gutiérrez E, Cachofeiro V, Martínez-Martínez E, Marín G, Olmos C, Carrión I, Gil S, Mahía P, Cobos MÁ, de Agustín A, and Luaces M

Abstract

Background: Over the past years, information about the crosstalk between the epicardial adipose tissue (EAT) and the cardiovascular system has emerged. Notably, in the context of acute myocardial infarction (AMI), EAT might have a potential role in the pathophysiology of ventricular structural changes and function, and the clinical evolution of patients. This study aims to assess the impact of EAT on morpho-functional changes in the left ventricle (LV) and the outcome of patients after an AMI., Methods: We studied prospectively admitted patients to our hospital with a first episode of AMI. All patients underwent percutaneous coronary intervention (PCI) during admission. Transthoracic echocardiography (TTE) was performed within 24-48 h after PCI, as well as blood samples to assess levels of galectin-3 (Gal-3). Cardiac magnetic resonance (CMR) was performed 5-7 days after PCI. Clinical follow-up was performed at 1 and 5 years after MI., Results: Mean age of our cohort ( n = 41) was 57.5 ± 10 years, and 38 (93%) were male. Nine patients had normal BMI, 15 had overweight (BMI 25-30), and 17 were obese (BMI > 30). Twenty three patients (56%) had ≥ 4 mm thickness of EAT measured with echo. In these patients, baseline left ventricular ejection fraction (LVEF) after AMI was significantly lower, as well as global longitudinal strain. EAT thickness ≥ 4 m patients presented larger infarct size, higher extracellular volume, and higher T1 times than patients with EAT < 4 mm. As for Gal-3, the median was 16.5 ng/mL [12.7-25.2]. At five-year follow-up 5 patients had major cardiac events, and all of them had EAT ≥ 4 mm., Conclusions: Patients with EAT >4 mm have worse LVEF and GLS, larger infarct size and longer T1 values after a MI, and higher levels of Gal-3. EAT >4 mm was an independent predictor of MACE at 5-year follow-up. EAT thickness is a feasible, noninvasive, low-cost parameter that might provide important information regarding the chronic inflammatory process in the myocardium after an infarction., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Islas, Gutiérrez, Cachofeiro, Martínez-Martínez, Marín, Olmos, Carrión, Gil, Mahía, Cobos, de Agustín and Luaces.)

Published
2022
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44. Mitochondrial Oxidative Stress Induces Cardiac Fibrosis in Obese Rats through Modulation of Transthyretin.

Author

Martínez-Martínez E, Fernández-Irigoyen J, Santamaría E, Nieto ML, Bravo-San Pedro JM, and Cachofeiro V

Subjects
Animals, Antioxidants metabolism, Antioxidants pharmacology, Diet, High-Fat adverse effects, Fibrosis, Male, Obesity complications, Obesity metabolism, Oxidative Stress, Proteomics, Rats, Rats, Wistar, Prealbumin metabolism, Ubiquinone metabolism, Ubiquinone pharmacology
Abstract

A proteomic approach was used to characterize potential mediators involved in the improvement in cardiac fibrosis observed with the administration of the mitochondrial antioxidant MitoQ in obese rats. Male Wistar rats were fed a standard diet (3.5% fat; CT) or a high-fat diet (35% fat; HFD) and treated with vehicle or MitoQ (200 μM) in drinking water for 7 weeks. Obesity modulated the expression of 33 proteins as compared with controls of the more than 1000 proteins identified. These include proteins related to endoplasmic reticulum (ER) stress and oxidative stress. Proteomic analyses revealed that HFD animals presented with an increase in cardiac transthyretin (TTR) protein levels, an effect that was prevented by MitoQ treatment in obese animals. This was confirmed by plasma levels, which were associated with those of cardiac levels of both binding immunoglobulin protein (BiP), a marker of ER stress, and fibrosis. TTR stimulated collagen I production and BiP in cardiac fibroblasts. This upregulation was prevented by the presence of MitoQ. In summary, the results suggest a role of TTR in cardiac fibrosis development associated with obesity and the beneficial effects of treatment with mitochondrial antioxidants.

Published
2022
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45. Mitochondrial Oxidative Stress Promotes Cardiac Remodeling in Myocardial Infarction through the Activation of Endoplasmic Reticulum Stress.

Author

Souza-Neto FV, Islas F, Jiménez-González S, Luaces M, Ramchandani B, Romero-Miranda A, Delgado-Valero B, Roldan-Molina E, Saiz-Pardo M, Cerón-Nieto MÁ, Ortega-Medina L, Martínez-Martínez E, and Cachofeiro V

Abstract

We have evaluated cardiac function and fibrosis in infarcted male Wistar rats treated with MitoQ (50 mg/kg/day) or vehicle for 4 weeks. A cohort of patients admitted with a first episode of acute MI were also analyzed with cardiac magnetic resonance and T1 mapping during admission and at a 12-month follow-up. Infarcted animals presented cardiac hypertrophy and a reduction in the left ventricular ejection fraction (LVEF) and E- and A-waves (E/A) ratio when compared to controls. Myocardial infarction (MI) rats also showed cardiac fibrosis and endoplasmic reticulum (ER) stress activation. Binding immunoglobulin protein (BiP) levels, a marker of ER stress, were correlated with collagen I levels. MitoQ reduced oxidative stress and prevented all these changes without affecting the infarct size. The LVEF and E/A ratio in patients with MI were 57.6 ± 7.9% and 0.96 ± 0.34, respectively. No major changes in cardiac function, extracellular volume fraction (ECV), or LV mass were observed at follow-up. Interestingly, the myeloperoxidase (MPO) levels were associated with the ECV in basal conditions. BiP staining and collagen content were also higher in cardiac samples from autopsies of patients who had suffered an MI than in those who had died from other causes. These results show the interactions between mitochondrial oxidative stress and ER stress, which can result in the development of diffuse fibrosis in the context of MI.

Published
2022
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46. Microsomal prostaglandin E synthase-1 is involved in the metabolic and cardiovascular alterations associated with obesity.

Author

Ballesteros-Martínez C, Rodrigues-Díez R, Beltrán LM, Moreno-Carriles R, Martínez-Martínez E, González-Amor M, Martínez-González J, Rodríguez C, Cachofeiro V, Salaices M, and Briones AM

Subjects
Adipose Tissue metabolism, Animals, Diet, High-Fat, Female, Fibrosis, Glucose metabolism, Humans, Inflammation metabolism, Lipids, Male, Mice, Mice, Inbred C57BL, Insulin Resistance, Obesity metabolism, Prostaglandin-E Synthases genetics, Prostaglandin-E Synthases metabolism
Abstract

Background and Purpose: Microsomal prostaglandin E synthase-1 (mPGES-1) is an inducible isomerase responsible for prostaglandin E 2 production in inflammatory conditions. We evaluated the role of mPGES-1 in the development and the metabolic and cardiovascular alterations of obesity., Experimental Approach: mPGES-1 +/+ and mPGES-1 -/- mice were fed with normal or high fat diet (HFD, 60% fat). The glycaemic and lipid profile was evaluated by glucose and insulin tolerance tests and colorimetric assays. Vascular function, structure and mechanics were assessed by myography. Histological studies, q-RT-PCR, and western blot analyses were performed in adipose tissue depots and cardiovascular tissues. Gene expression in abdominal fat and perivascular adipose tissue (PVAT) from patients was correlated with vascular damage., Key Results: Male mPGES-1 -/- mice fed with HFD were protected against body weight gain and showed reduced adiposity, better glucose tolerance and insulin sensitivity, lipid levels and less white adipose tissue and PVAT inflammation and fibrosis, compared with mPGES-1 +/+ mice. mPGES-1 knockdown prevented cardiomyocyte hypertrophy, cardiac fibrosis, endothelial dysfunction, aortic insulin resistance, and vascular inflammation and remodelling, induced by HFD. Obesity-induced weight gain and endothelial dysfunction of resistance arteries were ameliorated in female mPGES-1 -/- mice. In humans, we found a positive correlation between mPGES-1 expression in abdominal fat and vascular remodelling, vessel stiffness, and systolic blood pressure. In human PVAT, there was a positive correlation between mPGES-1 expression and inflammatory markers., Conclusions and Implications: mPGES-1 inhibition might be a novel therapeutic approach to the management of obesity and the associated cardiovascular and metabolic alterations., (© 2021 The Authors. British Journal of Pharmacology published by John Wiley & Sons Ltd on behalf of British Pharmacological Society.)

Published
2022
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47. Angiotensin II Promotes Skeletal Muscle Angiogenesis Induced by Volume-Dependent Aerobic Exercise Training: Effects on miRNAs-27a/b and Oxidant-Antioxidant Balance.

Author

Rodrigues LF, Pelozin BRA, da Silva Junior ND, Soci UPR, do Carmo EC, da Mota GFA, Cachofeiro V, Lahera V, Oliveira EM, and Fernandes T

Abstract

Aerobic exercise training (ET) produces beneficial adaptations in skeletal muscles, including angiogenesis. The renin-angiotensin system (RAS) is highly involved in angiogenesis stimuli. However, the molecular mechanisms underlying capillary growth in skeletal muscle induced by aerobic ET are not completely understood. This study aimed to investigate the effects of volume-dependent aerobic ET on skeletal muscle angiogenesis involving the expression of miRNAs-27a and 27b on RAS and oxidant-antioxidant balance. Eight-week-old female Wistar rats were divided into three groups: sedentary control (SC), trained protocol 1 (P1), and trained protocol 2 (P2). P1 consisted of 60 min/day of swimming, 5×/week, for 10 weeks. P2 consisted of the same protocol as P1 until the 8th week, but in the 9th week, rats trained 2×/day, and in the 10th week, trained 3×/day. Angiogenesis and molecular analyses were performed in soleus muscle samples. Furthermore, to establish ET-induced angiogenesis through RAS, animals were treated with an AT1 receptor blocker (losartan). Aerobic ET promoted higher VO 2 peak and exercise tolerance values. In contrast, miRNA-27a and -27b levels were reduced in both trained groups, compared with the SC group. This was in parallel with an increase in the ACE1/Ang II/VEGF axis, which led to a higher capillary-to-fiber ratio. Moreover, aerobic ET induced an antioxidant profile increasing skeletal muscle SOD2 and catalase gene expression, which was accompanied by high nitrite levels and reduced nitrotyrosine concentrations in the circulation. Additionally, losartan treatment partially re-established the miRNAs expression and the capillary-to-fiber ratio in the trained groups. In summary, aerobic ET promoted angiogenesis through the miRNA-27a/b-ACE1/Ang II/VEGF axis and improved the redox balance. Losartan treatment demonstrates the participation of RAS in ET-induced vascular growth. miRNAs and RAS components are promising potential targets to modulate angiogenesis for combating vascular diseases, as well as potential biomarkers to monitor training interventions and physical performance.

Published
2022
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48. Oxidative Stress in Obesity.

Author

Martínez-Martínez E and Cachofeiro V

Abstract

Obesity is defined by the World Health Organization (WHO) as abnormal or excessive fat accumulation that presents a health risk [...].

Published
2022
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49. Serum interleukin-6 levels predict kidney disease progression in diabetic nephropathy.

Author

Sanchez-Alamo B, Shabaka A, Cachofeiro V, Cases-Corona C, and Fernandez-Juarez G

Subjects
Disease Progression, Humans, Interleukin-6, Kidney, Diabetes Mellitus, Type 2 complications, Diabetes Mellitus, Type 2 diagnosis, Diabetic Nephropathies diagnosis, Diabetic Nephropathies etiology
Abstract

Background: Inflammation is a main mechanism for the pathogenesis and progression of diabetic kidney disease (DKD). Interleukin-6 (IL-6) is an important inflammatory mediator that is suggested to be involved in the pathogenesis of DKD. The aim of our study was to evaluate the association between IL-6 levels and progression of DKD in patients with type 2 diabetes mellitus. Materials an methods: IL-6 levels were measured at baseline and after 4 and 12 months in 70 patients included in a multi-center, randomized controlled clinical trial designed to compare the effect of RAS blockers in monotherapy to dual blockade for slowing the progression of DKD. The primary composite endpoint was > 50% increase in baseline serum creatinine, end-stage kidney disease (ESKD), or death., Results: The median follow-up was 36 months, during which 27 patients (38.6%) reached the primary endpoint. Baseline IL-6 levels correlated with TNF-α, C-reactive protein, and PTH levels. Survival analysis showed that patients with the highest IL-6 levels (> 4.84 pg/mL) reached the primary endpoint faster than the other two groups. Multivariate Cox regression analysis showed that baseline IL-6 levels > 4.84 pg/mL (HR 4.10, 95% CI 1.36 - 12.31) were a risk factor for reaching the primary endpoint adjusted for eGFR and proteinuria. Generalized linear mixed model analysis showed no effect on subsequent IL-6 levels either with RAS blockade monotherapy or dual blockade., Conclusion: These results suggest that treatment with RAS blockade does not influence IL-6 levels. IL-6 is independently associated with an increased risk for progression of DKD.

Published
2022
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50. The Interplay of Mitochondrial Oxidative Stress and Endoplasmic Reticulum Stress in Cardiovascular Fibrosis in Obese Rats.

Author

Souza-Neto FV, Jiménez-González S, Delgado-Valero B, Jurado-López R, Genty M, Romero-Miranda A, Rodríguez C, Nieto ML, Martínez-Martínez E, and Cachofeiro V

Abstract

We have evaluated the role of mitochondrial oxidative stress and its association with endoplasmic reticulum (ER) stress activation in the progression of obesity-related cardiovascular fibrosis. MitoQ (200 µM) was orally administered for 7 weeks to male Wistar rats that were fed a high-fat diet (HFD, 35% fat) or a control diet (CT, 3.5% fat). Obese animals presented cardiovascular fibrosis accompanied by increased levels of extracellular matrix proteins and profibrotic mediators. These alterations were associated with ER stress activation characterized by enhanced levels (in heart and aorta vs. CT group, respectively) of immunoglobulin binding protein (BiP; 2.1-and 2.6-fold, respectively), protein disulfide-isomerase A6 (PDIA6; 1.9-fold) and CCAAT-enhancer-binding homologous protein (CHOP; 1.5- and 1.8-fold, respectively). MitoQ treatment was able to prevent ( p < 0.05) these modifications at cardiac and aortic levels. MitoQ (5 nM) and the ER stress inhibitor, 4-phenyl butyric acid (4 µM), were able to block the prooxidant and profibrotic effects of angiotensin II (Ang II, 10 -6 M) in cardiac and vascular cells. Therefore, the data show a crosstalk between mitochondrial oxidative stress and ER stress activation, which mediates the development of cardiovascular fibrosis in the context of obesity and in which Ang II can play a relevant role.

Published
2021
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