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Heat shock protein 72 expression is not essential for exercise induced protection against infarction and apoptosis following ischemia‐reperfusion
Abstract   Peer reviewed

Heat shock protein 72 expression is not essential for exercise induced protection against infarction and apoptosis following ischemia‐reperfusion

John C Quindry, Karyn L Hamilton, Joel P French, Youngil Lee, Zsolt Murlasits, Nihal Tumer and Scott K Powers
The FASEB journal, Vol.20(4), p.A318
03/2006
DOI: https://doi.org/10.1096/fasebj.20.4.A318-a

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Abstract

Exercise provides protection against ischemia‐reperfusion (IR) induced injury and is associated with increased myocardial levels of heat shock protein 72 (HSP72). Whether HSP72 is essential for exercise induced protection against IR induced cell death is unknown. These experiments investigated the prevention of exercise induced increase in HSP72 on myocardial infarction and apoptosis following 50 min ischemia and 120 min reperfusion. Male rats remained sedentary or performed successive bouts of endurance exercise in cold (8°C) or warm (22°C) environments. Warm exercise resulted in elevated myocardial HSP72 content compared to cold exercise and sedentary conditions. Following in vivo myocardial IR, infarct size was reduced in both exercised groups compared to sedentary animals. Further, myocardial apoptosis, determined by (terminal deoxynucleotidyl transferase nick end labeling, TUNEL) was attenuated in both exercise treatments as compared to IRhearts from sedentary rats. Collectively, these findings indicate that HSP72 is not essential to achieve exercise induced cardioprotection against IR‐induced myocardial cell death. Further elucidation of the mechanisms responsible for exercise induced cardioprotection against apoptosis remains the focus of future investigations. Supported by NIH HL072789 (SKP), NIH HL074666 (JCQ)

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