Cardioselective Overexpression of HO-1 Prevents I/R-Induced Cardiac Dysfunction and Apoptosis
Document Type
Article
Publication Date
1-1-2002
Description
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 α-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.
Citation Information
Vulapalli, Sreesatya Raju; Chen, Zhongyi; Chua, Balvin H.L.; Wang, Tingchung; and Liang, Chang Seng. 2002. Cardioselective Overexpression of HO-1 Prevents I/R-Induced Cardiac Dysfunction and Apoptosis. American Journal of Physiology - Heart and Circulatory Physiology. Vol.283(2 52-2). https://doi.org/10.1152/ajpheart.00133.2002 PMID: 12124217 ISSN: 0363-6135