MiP2005: Session 8

Abstract without presentation                                                  Mitochondrial Physiology Network 10.9: 100 (2005) - download pdf

 

Mitochondrial mechanism of stress-induced cardiomyocyte injury.

Lingjia Qian, H Ren, J Gong, W Wang

Inst. Health Environmental Medicine, Tianjin 300050, China. - qianlj2000@hotmail.com

It is confirmed that stress induces cardiovascular dieases with cardiomyocyte injury, but its cellular and molecular mechanism remains unclear.  In the present study the changes of cardiac mitochondria of stressed rats were characterized to explore the influence of stress on mitochondrial function and its role in cardiomyocyte injury. The results showed that stress induced the increase of the respiratory control rate (RCR) and oxidative phosphorylation efficiency (P/O) in the mitochondria of cardiomyocytes in the time and dose dependent fashion, and resulted in the disorder of intracellular Ca2+ balance. The stress induced alteration of mitochondrial membrane permeability transition (MPT) was also found, which in turn led to the release of cytochrome c from mitochondria to cytosol and activated caspase cascade in cardiomyocytes. Stress also increased the Fas expression and activated the Fas pathway through acting on the mitochondrial MPT. Mechanism. Bcl-2 overexpression in cardiomyocyte protected the mitochondria from stress injury and reduced the cardiomyocyte death, including apoptosis and necrosis, induced by stress. Hsp70 also depressed the Fas–mitochondria pathway to decrease the death rate of cardiomyocyte under stress loading. As a conclusion it appears that the mitochondria play an important role in the mechanism of stress induced cardiomyocyte injury. Both Bcl-2 and Hsp70 seem the key regulators in the mitochondrial mechanism of stress induced cardiomyocyte apoptosis. These findings imply the possibility that regulating the expression of Bcl-2 or Hsp70 to protect mitochondria acts as a new therapeutic principle in cardiovascular diseases.

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