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Biochem Biophys Res Commun. 2010 Jun 25;397(2):270-6. doi: 10.1016/j.bbrc.2010.05.099. Epub 2010 May 24.

Mitofusin-2 protects against cold stress-induced cell injury in HEK293 cells.

Author information

1
Department of Occupational & Environmental Health, School of Public Health, Fourth Military Medical University, Xi'an 710032, China.

Abstract

Mitochondrial impairment is hypothesized to contribute to cell injury during cold stress. Mitochondria fission and fusion are closely related in the function of the mitochondria, but the precise mechanisms whereby these processes regulate cell injury during cold stress remain to be determined. HEK293 cells were cultured in a cold environment (4.0+/-0.1 degrees C) for 2, 4, 8, or 12h. Western blot analyses showed that these cells expressed decreased fission-related protein Drp1 and increased fusion-related protein Mfn2 at 4h; meanwhile, electron microscopy analysis revealed large and long mitochondrial morphology within these cells, indicating increased mitochondrial fusion. With silencing of Mfn2 but not of Mfn1 by siRNA promoted cold-stress-induced cell death with decreased ATP production in HEK293 cells. Our results show that increased expression of Mfn2 and mitochondrial fusion are important for mitochondrial function as well as cell survival during cold stress. These findings have important implications for understanding the mechanisms of mitochondrial fusion and fission in cold-stress-induced cell injury.

PMID:
20580691
DOI:
10.1016/j.bbrc.2010.05.099
[Indexed for MEDLINE]

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