期刊
MOLECULAR BIOLOGY REPORTS
卷 39, 期 4, 页码 3987-3993出版社
SPRINGER
DOI: 10.1007/s11033-011-1179-2
关键词
Heat shock; HSF1; ER stress; XBP1; eIF2 alpha
资金
- Ministry of Education, Culture, Sports, Science, Japan
- Grants-in-Aid for Scientific Research [21390334, 23591679, 23591399] Funding Source: KAKEN
Although heat stress induces a variety of illnesses, there have been few studies designed to uncover the molecular mechanisms underlining the illnesses. We here demonstrate that heat activates ER stress, which inhibits heat shock responses (HSR) via translational block. In heat-stressed rats, ER stress responses, as represented by eIF2 alpha phosphorylation and XBP1 splicing, occurred mainly in the cortex, where the HSR was substantially inhibited. Heat exposure also activated ER stress signals in primary cortical neurons. Since HSF1 knockdown enhanced heat-induced ER stress and subsequent cell death, HSR inhibition in turn augments ER stress, implying a vicious spiral of both stresses. Taken together, heat-induced ER stress impairs the HSR and enhances cell damage, thereby manifesting its unique effect on heat stress.
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