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Original Article |
1 Research Center for Cardiovascular Regenerative Medicine, Cardiovascular Institute and Fu Wai Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
* To whom correspondence should be addressed. E-mail: chenxifw{at}yahoo.com.cn.
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Abstract |
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In recent years, the understanding that regeneration progresses exist at the level of the
myocardium has placed stem cell research at the center stage in cardiology. Despite an
increasing interest in cell transplant research, relatively little is known about the biochemical regulation of the stem cells itself after transplanted to an ischemic heart. We demonstrated here, using rat mesenchymal stem cells (MSCs), that cells undergo caspase-dependent apoptosis in response to hypoxia and serum deprivation (SD), which are both components of ischemia in vivo. In particular, the treated cells exhibited mitochondrial dysfunction, including cytochrome C release, loss in 
m and Bax accumulation, but in a p53 independent manner. Although the cells treated by hypoxia/SD possess the activity of caspase-8, zIEDT-fmk, a specific caspase-8 inhibitor, failed to inhibit cell apoptosis induced in our system. Taken together, our findings indicate that MSCs are sensitive to hypoxia/SD stimuli that involve changes in mitochondrial integrity and function but potentially independent of caspase-8.
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