A protective role of 27-kDa heat shock protein in glucocorticoid-evoked apoptotic cell death of hippocampal progenitor cells.
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.
Son
Gi Hoon
GH
School of Biological Sciences, Seoul National University, Seoul 151-742, Republic of Korea.
Geum
Dongho
D
Chung
Sooyoung
S
Park
Eonyoung
E
Lee
Kun Ho
KH
Choi
Sukwoo
S
Kim
Kyungjin
K
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D015152:Blotting, Northern; D015153:Blotting, Western; D002460:Cell Line; D003907:Dexamethasone / Q000494:pharmacology*; D005434:Flow Cytometry; D006360:Heat-Shock Proteins / Q000096:biosynthesis / Q000502:physiology*; D006624:Hippocampus / Q000166:cytology*; D006801:Humans; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism; D013234:Stem Cells / Q000502:physiology*
D006360:Heat-Shock Proteins; D017382:Reactive Oxygen Species; D003907:Dexamethasone