The heat-induced gamma-H2AX response does not play a role in hyperthermic cell killing.

The goal of this study was to determine whether the heat-induced formation of gamma-H2AX foci is involved in hyperthermic cell killing. The heat-induced gamma-H2AX response was determined in cells exhibiting various degrees of heat sensitivity. The panel of cells tested included cells that are transiently thermotolerant, permanently heat resistant, permanently heat sensitive, and permanently resistant to oxidative stress. Cells exposed to non-thermal environmental conditions that lead to protection from, or sensitization to, heat were also tested. The heat sensitivity of cells in which H2AX was knocked out was also ascertained. The protein synthesis independent state of thermotolerance, but not the protein synthesis dependent state of thermotolerance, was found to be involved in the attenuation of the gamma-H2AX response in thermotolerant cells. The initial magnitude of the gamma-H2AX response was found to be the same in all cell lines with altered heat sensitivity. Furthermore, no differences in the resolution of gamma-H2AX foci were found among the cell lines tested. We also found that H2AX knock-out cells were not more heat sensitive. We conclude that the heat-induced gamma-H2AX response does not play a role in heat-induced cell killing, thereby adding further evidence that the heat-induced gamma-H2AX foci are not due to DNA double strand breaks.

Citation

Andrei Laszlo, Ilona Fleischer. The heat-induced gamma-H2AX response does not play a role in hyperthermic cell killing. International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group. 2009 May;25(3):199-209

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PMID: 19437236

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