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001-es BibID:	BIBFORM044733
Első szerző:	Vandenwijngaert, Sara
Cím:	Increased Cardiac Myocyte PDE5 Levels in Human and Murine Pressure Overload Hypertrophy Contribute to Adverse LV Remodeling / Sara Vandenwijngaert, Pokreisz Péter, Hadewich Hermans, Hilde Gillijns, Marijke Pellens, Noortje A. M. Bax, Giulia Coppiello, Wouter Oosterlinck, Balogh Ágnes, Papp Zoltán, Carlijn V. C. Bouten, Jozef Bartunek, Jan D'hooge, Aernout Luttun, Erik Verbeken, Marie Christine Herregods, Paul Herijgers, Kenneth D. Bloch, Stefan Janssens
Dátum:	2013
ISSN:	1932-6203
Megjegyzések:	BACKGROUND: The intracellular second messenger cGMP protects the heart under pathological conditions. We examined expression of phosphodiesterase 5 (PDE5), an enzyme that hydrolyzes cGMP, in human and mouse hearts subjected to sustained left ventricular (LV) pressure overload. We also determined the role of cardiac myocyte-specific PDE5 expression in adverse LV remodeling in mice after transverse aortic constriction (TAC). METHODOLOGY/PRINCIPAL FINDINGS: In patients with severe aortic stenosis (AS) undergoing valve replacement, we detected greater myocardial PDE5 expression than in control hearts. We observed robust expression in scattered cardiac myocytes of those AS patients with higher LV filling pressures and BNP serum levels. Following TAC, we detected similar, focal PDE5 expression in cardiac myocytes of C57BL/6NTac mice exhibiting the most pronounced LV remodeling. To examine the effect of cell-specific PDE5 expression, we subjected transgenic mice with cardiac myocyte-specific PDE5 overexpression (PDE5-TG) to TAC. LV hypertrophy and fibrosis were similar as in WT, but PDE5-TG had increased cardiac dimensions, and decreased dP/dtmax and dP/dtmin with prolonged tau (P<0.05 for all). Greater cardiac dysfunction in PDE5-TG was associated with reduced myocardial cGMP and SERCA2 levels, and higher passive force in cardiac myocytes in vitro. CONCLUSIONS/SIGNIFICANCE: Myocardial PDE5 expression is increased in the hearts of humans and mice with chronic pressure overload. Increased cardiac myocyte-specific PDE5 expression is a molecular hallmark in hypertrophic hearts with contractile failure, and represents an important therapeutic target.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Plos One. - 8 : 3 (2013), p. 1-9. -
További szerzők:	Pokreisz Péter Hermans, Hadewich Gillijns, Hilde Pellens, Marijke Bax, Noortje A. M. Coppiello, Giulia Oosterlinck, Wouter Balogh Ágnes (1984-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász) Bouten, Carlijn V. C. Bartunek, Jozef D'hooge, Jan Luttun, Aernout Verbeken, Erik Herregods, Marie Christine Herijgers, Paul Bloch, Kenneth D. Janssens, Stefan
Pályázati támogatás:	TÁMOP-4.2.2.A-11/1/KONV-2012-0045 TÁMOP
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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