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

Gi Hoon Son; Dongho Geum; Sooyoung Chung; Eonyoung Park; Kun Ho Lee; Sukwoo Choi; Kyungjin Kim

doi:10.1016/j.bbrc.2005.10.152

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

Gi Hoon Son, Dongho Geum, Sooyoung Chung, Eonyoung Park, Kun Ho Lee, Sukwoo Choi, Kyungjin Kim

Brain & Cognitive Sciences

Research output: Contribution to journal › Article › peer-review

30 Scopus citations

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.

Original language	English
Pages (from-to)	1751-1758
Number of pages	8
Journal	Biochemical and Biophysical Research Communications
Volume	338
Issue number	4
DOIs	https://doi.org/10.1016/j.bbrc.2005.10.152
State	Published - 30 Dec 2005

Bibliographical note

Funding Information:
This research was supported by a grant from Brain Research Center of the 21st Century Frontier Research Program funded by the Ministry of Science and Technology, the Republic of Korea. G.H. Son, S. Chung, E. Park, and K.H. Lee were supported by Brain Korea 21 Research Fellowship from the Korea Ministry of Education and Human Resources. We appreciate the services of Biomedical English Editing Service (Portland, OR).

Keywords

Apoptosis
Glucocorticoid
HSP27
HiB5
Hippocampal progenitor

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title = "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.",

keywords = "Apoptosis, Glucocorticoid, HSP27, HiB5, Hippocampal progenitor",

author = "Son, {Gi Hoon} and Dongho Geum and Sooyoung Chung and Eonyoung Park and Lee, {Kun Ho} and Sukwoo Choi and Kyungjin Kim",

note = "Funding Information: This research was supported by a grant from Brain Research Center of the 21st Century Frontier Research Program funded by the Ministry of Science and Technology, the Republic of Korea. G.H. Son, S. Chung, E. Park, and K.H. Lee were supported by Brain Korea 21 Research Fellowship from the Korea Ministry of Education and Human Resources. We appreciate the services of Biomedical English Editing Service (Portland, OR).",

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T1 - A protective role of 27-kDa heat shock protein in glucocorticoid-evoked apoptotic cell death of hippocampal progenitor cells

AU - Son, Gi Hoon

AU - Geum, Dongho

AU - Chung, Sooyoung

AU - Park, Eonyoung

AU - Lee, Kun Ho

AU - Choi, Sukwoo

AU - Kim, Kyungjin

N1 - Funding Information: This research was supported by a grant from Brain Research Center of the 21st Century Frontier Research Program funded by the Ministry of Science and Technology, the Republic of Korea. G.H. Son, S. Chung, E. Park, and K.H. Lee were supported by Brain Korea 21 Research Fellowship from the Korea Ministry of Education and Human Resources. We appreciate the services of Biomedical English Editing Service (Portland, OR).

PY - 2005/12/30

Y1 - 2005/12/30

N2 - 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.

AB - 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.

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

Abstract

Bibliographical note

Keywords

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