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THE STEM CELL NICHE

Hypoxia and Serum Deprivation-Induced Apoptosis in Mesenchymal Stem Cells

Research Center for Cardiovascular Regenerative Medicine, Cardiovascular Institute and Fu Wai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, People’s Republic of China

Key Words. Mesenchymal stem cells • Hypoxia/serum deprivation • Apoptosis • Mitochondria

Correspondence: Xi Chen, Ph.D., and Shengshou Hu, M.D., Research Center for Cardiovascular Regenerative Medicine, Cardiovascular Institute and Fu Wai Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100037, People’s Republic of China. Telephone: 086-10-68331762; Fax: 086-10-68331762; e-mail: chenxifw{at}yahoo.com.cn and huss{at}163bj.com

In recent years, the understanding that regeneration progresses 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 cell itself after transplantation into 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 are potentially independent of caspase-8.

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