IR@PKUHSC  > 北京大学基础医学院  > 神经生物学系
学科主题基础医学
Cycloheximide and actinomycin D delay death and affect bcl-2, bax, and ice gene expression in astrocytes under in vitro ischemia
Yu, ACH; Yung, HW; Hui, MHK; Lau, LT; Chen, XQ; Collins, RA
关键词actinomycin D apoptosis astrocytes cycloheximide bcl-2 Bax ice ischemia
刊名JOURNAL OF NEUROSCIENCE RESEARCH
2003-10-15
DOI10.1002/jnr.10742
74期:2页:318-325
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Neurosciences
研究领域[WOS]Neurosciences & Neurology
关键词[WOS]SENSORY NEURON SURVIVAL ; NECROSIS-FACTOR-ALPHA ; PRIMARY CULTURES ; MESSENGER-RNA ; CELL-DEATH ; PROTOONCOGENE BCL-2 ; CONVERTING-ENZYME ; PROTEIN-SYNTHESIS ; INDUCED APOPTOSIS ; INJURY
英文摘要

An in vitro ischemia model was established and the effect of the metabolic inhibitors cycloheximide (CHX) and actinomycin D (ActD) on apoptosis in astrocytes under ischemia studied. CHX decreased by 75% the number of cells dying after 6 hr of ischemia compared with control cultures. TdT-mediated dUTP nick end labelling (TUNEL) staining of comparable cultures was reduced by 40%. ActD decreased cell death by 60% compared with controls. The number of TUNEL-positive cells was reduced by 38%. The nuclear shrinkage in TUNEL-positive astrocytes in control cultures did not occur in ActD-treated astrocytes, indicating that nuclear shrinkage and DNA fragmentation during apoptosis are two unrelated processes. Expression of bcl-2 (alpha and beta), bax, and Ice in astrocytes under similar ischemic conditions, as measured by quantitative reverse transcription-polymerase chain reaction, indicated that ischemia down-regulated bcl-2 (alpha and beta) and bax. Ice was initially down-regulated from 0 to 4 hr, before returning to control levels after 8 hr of ischemia. ActD decreased the expression of these genes. CHX reduced the expression of bcl-2 (alpha and beta) but increased bax and Ice expression. It is hypothesized that the balance of proapoptotic (Bad, Bax) and antiapoptotic (Bcl-2, Bcl-XI) proteins determines apoptosis. The data suggest that the ratio of Bcl-2/Bad in astrocytes following ActD and CHX treatment does not decrease as much in untreated cells during ischemia. Our data indicate that it is the ratio of Bcl-2 family members that plays a critical role in determining ischemia-induced apoptosis. It is also important to note that ischemia-induced apoptosis involves the regulation of RNA and protein synthesis. (C) 2003 Wiley-Liss, Inc.

语种英语
WOS记录号WOS:000185692900016
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被引频次:9[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/64569
专题北京大学基础医学院_神经生物学系
作者单位1.Peking Univ, Neurosci Res Inst, Beijing 100083, Peoples R China
2.Peking Univ, Hlth Sci Ctr, Dept Neurobiol, Beijing 100871, Peoples R China
3.Hong Kong DNA Chips Ltd, Hong Kong, Hong Kong, Peoples R China
4.Hong Kong Univ Sci & Technol, Dept Biol, Hong Kong, Hong Kong, Peoples R China
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Yu, ACH,Yung, HW,Hui, MHK,et al. Cycloheximide and actinomycin D delay death and affect bcl-2, bax, and ice gene expression in astrocytes under in vitro ischemia[J]. JOURNAL OF NEUROSCIENCE RESEARCH,2003,74(2):318-325.
APA Yu, ACH,Yung, HW,Hui, MHK,Lau, LT,Chen, XQ,&Collins, RA.(2003).Cycloheximide and actinomycin D delay death and affect bcl-2, bax, and ice gene expression in astrocytes under in vitro ischemia.JOURNAL OF NEUROSCIENCE RESEARCH,74(2),318-325.
MLA Yu, ACH,et al."Cycloheximide and actinomycin D delay death and affect bcl-2, bax, and ice gene expression in astrocytes under in vitro ischemia".JOURNAL OF NEUROSCIENCE RESEARCH 74.2(2003):318-325.
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