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Regulation of Heat Stress by HSF1 and GR

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Technical Report,15 Aug 2014,14 Aug 2015

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Henry M. Jackson Foundation for the Advancement of Military Medicine Bethesda United States

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The purpose of this project is to examine how activation of two cellular defense mechanisms mediated by heat shock transcription factor 1 HSF1 and glucocorticoid receptor GR is associated with heat tolerance and heat acclimation. In this first annual period, our major effort focused on examining effects of heat acclimation on activation of the two systems involving HSF1 and GR in cultured muscle cells. Based on our preliminary data, heat-acclimatized cells showed greater resistance against heat stress compared to unacclimatized ones. Heat-acclimatized cells were associated with significant translocation of both HSF1 and GR from the cytosol to nucleus and mitochondria, which was not observed in unacclimatized ones. We also found that heat-induced damage developed concurrently with mitochondrial dysfunction in muscle cells. Inhibition of dynamin-like protein 1 prevented mitochondrial fragmentation and improved viability of muscle cells during heat exposure. These preliminary results suggest that HSF1 and GR systems are involved in HA and mitochondrial integrity is central to resistance of muscle cells against heat-induced injury.

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