Open AccessFibroblast growth factor 2 is an essential cardioprotective factor in a closed‐chest model of cardiac ischemia‐reperfusion injury
Author(s) -
House Stacey L.,
Wang Joy,
Castro Angela M.,
Weinheimer Carla,
Kovacs Attila,
Ornitz David M.
Publication year - 2015
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.12278
Subject(s) - medicine , myocardial infarction , cardiology , reperfusion injury , cardiac function curve , ischemia , in vivo , fibroblast growth factor , endogeny , infarction , anesthesia , heart failure , biology , receptor , microbiology and biotechnology
Fibroblast growth factor 2 ( FGF 2) is cardioprotective in in vivo models of myocardial infarction; however, whether FGF 2 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 FGF 2, 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 FGF 2 in a clinically relevant, in vivo, closed‐chest regional cardiac IR injury model that mimics acute myocardial infarction.