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Am J Physiol Heart Circ Physiol 283: H688-H694, 2002; doi:10.1152/ajpheart.00133.2002
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Vol. 283, Issue 2, H688-H694, August 2002

Cardioselective overexpression of HO-1 prevents I/R-induced cardiac dysfunction and apoptosis

Sreesatya Raju Vulapalli1, Zhongyi Chen3, Balvin H. L. Chua3, Tingchung Wang2, and Chang-Seng Liang1

1 Cardiology Unit, Department of Medicine, 2 Department of Surgery, University of Rochester School of Medicine, Rochester, New York 14642; and 3 Cecile Cox Quillen Laboratory of Geriatrics, James H. Quillen School of Medicine, East Tennessee State University and James H. Quillen Veterans Affairs Medical Center, Johnson City, Tennessee 37614

Heme oxygenase (HO)-1 converts heme to bilirubin, carbon monoxide, and iron. Our prior work has suggested a cardioprotective role for HO-1 in heart failure. To test whether HO-1 (heat shock protein 32) prevents cardiomyocyte apoptosis and cardiac dysfunction after ischemia-reperfusion (I/R), we generated transgenic mice overexpressing HO-1 in the heart under the control of the alpha -myosin heavy chain promoter. HO-1 transcript and protein increased markedly in the heart only. In an isolated heart preparation, we observed an enhanced functional recovery during reperfusion after ischemia in the transgenic hearts compared with nontransgenic controls. I/R injury was also performed in intact animals by coronary ligation and reperfusion to assess the protective role of HO-1 overexpression on heart apoptosis. HO-1 overexpression reduced cardiac apoptosis, as evidenced by fewer terminal deoxynucleodidyl transferase-mediated dUTP nick-end labeling-positive or in situ oligo ligation-positive myocytes, compared with nontransgenic mice. Our results indicate that cardioselective overexpression of HO-1 exerts a cardioprotective effect after myocardial I/R in mice, and this effect is probably mediated via an antiapoptotic action of HO-1.

heat shock protein 32; oxidative stress; myocardial protection; transgenic mice; coronary ligation


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