Attenuating ischemia-induced H9c2 myoblasts apoptosis by therapeutic hypothermia.
Although inducing mild hypothermia (32 degrees C) in animal models of cardiac arrest with highly attenuated cardiac and neurological injury, the protective effects of hypothermia molecular mechanisms were not fully elucidated, and thus, were examined here on the H9c2 rat ventricular myoblasts that underwent cell loss as well as apoptosis in conditions of simulated ischemia, represented by serum withdrawal plus hypoxia. The H9c2 cells apoptosis was evidenced by flow cytometry-, DNA fragmentation-, and caspase 3 activation-increased apoptotic cells (Annexin-V positive and propidium iodide negative). For the simulated ischemia, both cell loss and apoptosis of these cardiomyoblasts were associated with downregulated small molecular weight proteins (heat shock protein 20, heat shock protein 27, and alphaB-crystallin). Mild hypothermia significantly reduced the ischemia-induced apoptosis, small molecular weight proteins downregulation, and cell viability cut. Conclusively, hypothermia may inhibit simulated ischemia-induced apoptosis in cardiomyocytes by restoring normal small molecular weight proteins expression.
Lin
Cheng-Hsin
CH
Graduate Institute of Clinical Medicine and Department of Surgery, National Taiwan University School of Medicine, Taipei, Taiwan.
Wu
Wen-Shiann
WS
Lin
Mao-Tsun
MT
Liu
Wen-Ping
WP
Hsu
Ron-Bin
RB
Chang
Ching-Ping
CP
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D015687:Cell Hypoxia / Q000502:physiology; D002460:Cell Line; D002470:Cell Survival / Q000502:physiology; D053938:DNA Fragmentation; D007036:Hypothermia, Induced / Q000009:adverse effects; D032446:Myoblasts / Q000378:metabolism* / Q000473:pathology; D051381:Rats