Heat stress downregulates FLIP and sensitizes cells to Fas receptor-mediated apoptosis |
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Authors: | Tran S E F Meinander A Holmström T H Rivero-Müller A Heiskanen K M Linnau E K Courtney M J Mosser D D Sistonen L Eriksson J E |
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Institution: | Turku Centre for Biotechnology, Department of Biology, Abo Akademi University and University of Turku, Turku, Finland. |
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Abstract: | The heat shock response and death receptor-mediated apoptosis are both key physiological determinants of cell survival. We found that exposure to a mild heat stress rapidly sensitized Jurkat and HeLa cells to Fas-mediated apoptosis. We further demonstrate that Hsp70 and the mitogen-activated protein kinases, critical molecules involved in both stress-associated and apoptotic responses, are not responsible for the sensitization. Instead, heat stress on its own induced downregulation of FLIP and promoted caspase-8 cleavage without triggering cell death, which might be the cause of the observed sensitization. Since caspase-9 and -3 were not cleaved after heat shock, caspase-8 seemed to be the initial caspase activated in the process. These findings could help understanding the regulation of death receptor signaling during stress, fever, or inflammation. |
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