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A protective role of 27-kDa heat shock protein in glucocorticoid-evoked apoptotic cell death of hippocampal progenitor cells.

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.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Son GH,Geum D,Chung S,Park E,Lee KH,Choi S,Kim K

doi

10.1016/j.bbrc.2005.10.152

subject

Has Abstract

pub_date

2005-12-30 00:00:00

pages

1751-8

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(05)02446-0

journal_volume

338

pub_type

杂志文章

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