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Articles in PresS, published online ahead of print October 31, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00777.2002
Submitted on September 5, 2002
Accepted on October 24, 2002
1 Department s of Medicine (Molecular Cardiology), Albert Einstein College of Medicine, Bronx, NY, USA; Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY, USA
2 Division of Cardiovascular Research, St. Elizabeth's Medical Center, Boston, MA, USA
3 Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA, USA
4 Department of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA; Department s of Medicine (Molecular Cardiology), Albert Einstein College of Medicine, Bronx, NY, USA
* To whom correspondence should be addressed. E-mail: kitsis{at}aecom.yu.edu.
Fas is a widely expressed cell surface receptor that can initiate apoptosis when activated by its ligand (FasL). While Fas abundance on cardiac myocytes increases in response to multiple pathological stimuli, direct evidence supporting its role in the pathogenesis of heart disease is lacking. Moreover, controversy exists even as to whether Fas activation induces apoptosis in cardiac myocytes. In this study, we show that adenoviral overexpression of FasL, but not 
-galactosidase, results in marked apoptosis both in cultures of primary neonatal cardiac myocytes and in the myocardium of intact adult rats. Myocyte killing by FasL is a specific event, as it does not occur in lpr mice that lack functional Fas. To assess the contribution of the Fas pathway to myocardial infarction in vivo, lpr mice were subjected to 30 minutes of ischemia followed by 24 hours of reperfusion. As compared with wild type mice, lpr mice exhibited infarcts that were 62.3% smaller with 63.8% less myocyte apoptosis. These data provide direct evidence that activation of Fas can induce apoptosis in cardiac myocytes and that Fas is a critical mediator of myocardial infarction due to ischemia/reperfusion in vivo.
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