Bcl-2 family gene products in cerebral ischemia and traumatic brain injury

被引:93
作者
Graham, SH
Chen, J
Clark, RSB
机构
[1] Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15213 USA
[2] Univ Pittsburgh, Sch Med, Dept Anesthesiol & Crit Care Med, Pittsburgh, PA 15213 USA
[3] Univ Pittsburgh, Sch Med, Dept Pediat, Pittsburgh, PA 15213 USA
[4] Vet Affairs Pittsburgh Hlth Ctr, Ctr Geriatr Res Educ & Clin, Pittsburgh, PA USA
关键词
apoptosis; bax; bcl-2; bcl-w; bcl-x; bid; cerebral ischemia; programmed cell death; traumatic brain injury;
D O I
10.1089/neu.2000.17.831
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
The proto-oncogene bcl-2 plays a key role in regulating programmed cell death in neurons, The present review discusses the mechanisms by which bcl-2 family genes regulate programmed cell death, and their role in controlling cell death in cerebral ischemia and traumatic brain, Expression of several bcl-2 family members is altered in brain tissues after ischemia and trauma, suggesting that bcl-2 family genes could play a role in determining the fate of injured neurons. Furthermore, alteration of expression of bcl-2 family genes using transgenic approaches, viral vectors, or anti-sense oligonucleotides modifies neuronal cell death and neurological outcome after injury, These data suggest that the activity of bcl-2 family gene products participates in determining cellular and neurologic outcomes in ischemia and trauma, Strategies that either mimic the death-suppressor effects or inhibit the death-promoter effects of bcl-2 family gene products may improve outcome after ischemia and trauma.
引用
收藏
页码:831 / 841
页数:11
相关论文
共 95 条
  • [21] Caspases: the executioners of apoptosis
    Cohen, GM
    [J]. BIOCHEMICAL JOURNAL, 1997, 326 : 1 - 16
  • [22] PROGRAMMED CELL-DEATH BY BCL-2-DEPENDENT AND INDEPENDENT MECHANISMS IN B-LYMPHOMA CELLS
    CUENDE, E
    ALESMARTINEZ, JE
    DING, LY
    GONZALEZGARCIA, M
    MARTINEZA, C
    NUNEZ, G
    [J]. EMBO JOURNAL, 1993, 12 (04) : 1555 - 1560
  • [23] Cloning and expression of the programmed cell death regulator Bad in the rat brain
    D'Agata, V
    Magro, G
    Travali, S
    Musco, S
    Cavallaro, S
    [J]. NEUROSCIENCE LETTERS, 1998, 243 (1-3) : 137 - 140
  • [24] Caspase pathways, neuronal apoptosis, and CNS injury
    Eldadah, BA
    Faden, AI
    [J]. JOURNAL OF NEUROTRAUMA, 2000, 17 (10) : 811 - 829
  • [25] A caspase-activated DNase that degrades DNA during apoptosis, and its inhibitor ICAD
    Enari, M
    Sakahira, H
    Yokoyama, H
    Okawa, K
    Iwamatsu, A
    Nagata, S
    [J]. NATURE, 1998, 391 (6662) : 43 - 50
  • [26] Bax-induced cytochrome C release from mitochondria is independent of the permeability transition pore but highly dependent on Mg2+ ions
    Eskes, R
    Antonsson, B
    Osen-Sand, A
    Montessuit, S
    Richter, C
    Sadoul, R
    Mazzei, G
    Nichols, A
    Martinou, JC
    [J]. JOURNAL OF CELL BIOLOGY, 1998, 143 (01) : 217 - 224
  • [27] CLONING OF A BCL-2 HOMOLOG BY INTERACTION WITH ADENOVIRUS E1B 19K
    FARROW, SN
    WHITE, JHM
    MARTINOU, I
    RAVEN, T
    PUN, KT
    GRINHAM, CJ
    MARTINOU, JC
    BROWN, R
    [J]. NATURE, 1995, 374 (6524) : 731 - 733
  • [28] Mitochondrial participation in ischemic and traumatic neural cell death
    Fiskum, G
    [J]. JOURNAL OF NEUROTRAUMA, 2000, 17 (10) : 843 - 855
  • [29] PREVENTION OF PROGRAMMED CELL-DEATH OF SYMPATHETIC NEURONS BY THE BCL-2 PROTOONCOGENE
    GARCIA, I
    MARTINOU, I
    TSUJIMOTO, Y
    MARTINOU, JC
    [J]. SCIENCE, 1992, 258 (5080) : 302 - 304
  • [30] Altered expression of bcl-2, bcl-X, bax, and c-fos colocalizes with DNA fragmentation and ischemic cell damage following middle cerebral artery occlusion in rats
    Gillardon, F
    Lenz, C
    Waschke, KF
    Krajewski, S
    Reed, JC
    Zimmermann, M
    Kuschinsky, W
    [J]. MOLECULAR BRAIN RESEARCH, 1996, 40 (02): : 254 - 260