Abstract 19009: Increased Endogenous C-kit + Cardiac Stem Cells Diminish Myocardial Infarction Damage in S-nitrosoglutathione Reductase Mice

• Published in: Circulation (New York, N.Y.) N.Y.), 2012-11, Vol.126 (suppl_21)
• Main Authors: Paulino, Ellena C, Hatzistergos, Konstantinos E, Takeuchi, Lauro M, Kanashiro-Takeuchi, Rosemeire M, Balkan, Wayne, Hare, Joshua M
• Format: Article
• Language: English
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/circ.126.suppl_21.A19009

Abstract only Background. Cardiac tissue has endogenous cardiac stem cells (CSCs), which proliferate after myocardial infarction (MI) to support cardiac repair. As mice deficient in S-nitrosoglutathione reductase (GSNOR −/− ), an enzyme regulating S-nitrosothiol turnover, have preserved cardiac function after MI, we hypothesized that GSNOR −/− mice have higher levels of endogenous c-kit + CSCs post-MI. Methods. GSNOR −/− and WT (C57BL/6) mice were infarcted by permanent occlusion of the left anterior descending coronary artery. Cardiac performance was assessed by serial echocardiography. Histological sections were analyzed for infarct size and endogenous c-kit + /CD45 - CSCs were quantified by immunostaining. Results. There was no difference in ejection fraction (EF%) or endocardial volume (EDV, ESV) at baseline or 1 week post-MI, but at 8 weeks, EF% was improved (30.4±2.2 vs. 21.4±2.8, p