Fibroblast growth factor 2 is an essential cardioprotective factor in a closed‐chest model of cardiac ischemia‐reperfusion injury

Physiological Reports

Stacey L. House²  Joy Wang²  Angela M. Castro³  Carla Weinheimer¹  Attila Kovacs¹ 

[1] Center for Cardiovascular Research, Department of Medicine, Washington University in St. Louis School of Medicine, St. Louis, Missouri, USA;Division of Emergency Medicine, Washington University in St. Louis School of Medicine, St. Louis, Missouri, USA;Department of Developmental Biology, Washington University in St. Louis School of Medicine, St. Louis, Missouri, USA

关键词: Cardiac repair;    cardioprotection;    FGF2;    fibroblast growth factor;    ischemia‐reperfusion injury;    myocardial infarction;   

DOI  :  10.14814/phy2.12278

来源: Wiley

【 摘 要 】

Abstract

Fibroblast growth factor 2 (FGF2) is cardioprotective in in vivo models of myocardial infarction; however, whether FGF2 has a protective role in in vivo ischemia-reperfusion (IR) injury, a model that more closely mimics acute myocardial infarction in humans, is not known. To assess the cardioprotective efficacy of endogenous FGF2, mice lacking a functional Fgf2 gene (Fgf2^−/−) and wild-type controls were subjected to closed-chest regional cardiac IR injury (90 min ischemia, 7 days reperfusion). Fgf2^−/− mice had significantly increased myocardial infarct size and significantly worsened cardiac function compared to wild-type controls at both 1 and 7 days post-IR injury. Pathophysiological analysis showed that at 1 day after IR injury Fgf2^−/− mice have worsened cardiac strain patterns and increased myocardial cell death. Furthermore, at 7 days post-IR injury, Fgf2^−/− mice showed a significantly reduced cardiac hypertrophic response, decreased cardiac vessel density, and increased vessel diameter in the peri-infarct area compared to wild-type controls. These data reveal both acute cardioprotective and a longer term proangiogenic potential of endogenous FGF2 in a clinically relevant, in vivo, closed-chest regional cardiac IR injury model that mimics acute myocardial infarction.

【 授权许可】

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© 2015 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.

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