Characterization of hypothermia-induced cellular stress response in mouse tissues.
Cells respond to adverse environmental conditions by expressing heat shock proteins, which serve to protect cells from harmful effects of the stress conditions. In this study we demonstrated that mice subjected to whole body hypothermia induced the cellular stress response, resulting in the increased expression of hsp72 mRNA in brain, heart, kidney, liver, and lung. We performed a detailed analysis of the major parameters of the stress response and found that cold induction of hsp expression is mediated by heat shock factor 1 (HSF1), which is also responsible for heat induction of the cellular stress response. However, there are differences in the mechanisms of HSF1 activation by hypothermia versus hyperthermia, as hypothermia does not cause the hyperphosphorylation of HSF1 that is characteristic of heat-activated HSF1.
Cullen
K E
KE
Department of Biochemistry, Chandler Medical Center, University of Kentucky, Lexington, Kentucky 40536-0084, USA.
Sarge
K D
KD
D000818:Animals; D001921:Brain / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism*; D000076249:Heat Shock Transcription Factors; D006360:Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism*; D007035:Hypothermia / Q000378:metabolism / Q000473:pathology*; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D010766:Phosphorylation; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D014157:Transcription Factors
D004268:DNA-Binding Proteins; D000076249:Heat Shock Transcription Factors; D006360:Heat-Shock Proteins; D012333:RNA, Messenger; D014157:Transcription Factors