A protective role of 27-kDa heat shock protein in glucocorticoid-evoked apoptotic cell death of hippocampal progenitor cells
- Authors
- Son, GH; Geum, D; Chung, S; Park, E; Lee, KH; Choi, S; Kim, K
- Issue Date
- 30-12월-2005
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- HSP27; glucocorticoid; apoptosis; hippocampal progenitor; HiB5
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.338, no.4, pp.1751 - 1758
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 338
- Number
- 4
- Start Page
- 1751
- End Page
- 1758
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/123201
- DOI
- 10.1016/j.bbrc.2005.10.152
- ISSN
- 0006-291X
- Abstract
- Hippocampus is one of the most vulnerable tissues to glucocorticoid (GC). In the present study, we demonstrate that dexamethasone (DEX), a synthetic GC, induces apoptotic cell death in hippocampal progenitor HiB5 cells without any additional insult. Interestingly, expression of 27-kDa heat shock protein (HSP27) was markedly induced by DEX in time- and dose-dependent manners. This induction was dependent on the production of reactive oxygen species (ROS), suggesting that DEX-evoked oxidative damage to HiB5 cells is responsible for the HSP27 induction. To evaluate a possible role of HSP27, we generated two mutant HiB5 cell lines, in which expression of HSP27 was inhibited or enhanced by the over-expression of HSP27 cDNA with antisense or sense orientation (AS-HSP27 and S-HSP27, respectively). DEX-induced apoptotic cell population was significantly increased in AS-HSP27 HiB5 cells and evidently decreased in S-HSP27 cells. These results indicate that HSP27 protects hippocampal progenitor cells from GC-induced apoptotic cell death. (c) 2005 Elsevier Inc. All rights reserved.
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