BCL-2 IS EXPRESSED IN NEURONS THAT SURVIVE FOCAL ISCHEMIA IN THE RAT

被引:161
作者
CHEN, J
GRAHAM, SH
CHAN, PH
LAN, JQ
ZHOU, RL
SIMON, RP
机构
[1] VET ADM MED CTR,NEUROL SERV 127,PITTSBURGH,PA 15240
[2] UNIV CALIF SAN FRANCISCO,DEPT NEUROL,SAN FRANCISCO,CA 94143
[3] UNIV PITTSBURGH,SCH MED,DEPT NEUROL,PITTSBURGH,PA 15261
关键词
BCL-2; CEREBRAL ISCHEMIA; APOPTOSIS; NEURONS; MICROGLIA; ASTROCYTES;
D O I
10.1097/00001756-199501000-00040
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
EXPRESSION of the proto-oncogene bcl-2 prevents programmed cell death in vitro, but it is not known whether bcl-2 plays a role in determining cell survival after cerebral ischemia. Using immunohistochemistry and Western blot analysis, bcl-2 protein expression was studied in the rat brain 24 h following 60 or 120 min of temporary focal ischemia. Sixty minutes of ischemia induced bcl-2 protein in neurons throughout the frontoparietal cortex in noninfarcted regions, whereas 120 min of ischemia induced bcl-2 in neurons only just outside the margin of the infarction. bcl-2 protein was also induced in glial cells, mainly microglia, border zone of the infarction. In the infarcted regions of caudate and cortex, bcl-2 protein was exclusively induced in endothelial cells and the vessel walls. Western blot revealed a characteristic single band at 26 kDa only in ischemic samples. These data show that bcl-2 is induced in sublethally injured cells and suggest that bcl-2 could play a role in determining cell survival in cerebral ischemia.
引用
收藏
页码:394 / 398
页数:5
相关论文
共 24 条
[11]   INDUCTION OF 70-KDA HEAT-SHOCK PROTEIN AND HSP70 MESSENGER-RNA FOLLOWING TRANSIENT FOCAL CEREBRAL-ISCHEMIA IN THE RAT [J].
KINOUCHI, H ;
SHARP, FR ;
HILL, MP ;
KOISTINAHO, J ;
SAGAR, SM ;
CHAN, PH .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1993, 13 (01) :105-115
[12]   DISTRIBUTION OF THE 72-KD HEAT-SHOCK PROTEIN AS A FUNCTION OF TRANSIENT FOCAL CEREBRAL-ISCHEMIA IN RATS [J].
LI, Y ;
CHOPP, M ;
GARCIA, JH ;
YOSHIDA, Y ;
ZHANG, ZG ;
LEVINE, SR .
STROKE, 1992, 23 (09) :1292-1298
[13]   EVIDENCE SUPPORTING A ROLE FOR PROGRAMMED CELL-DEATH IN FOCAL CEREBRAL-ISCHEMIA IN RATS [J].
LINNIK, MD ;
ZOBRIST, RH ;
HATFIELD, MD .
STROKE, 1993, 24 (12) :2002-2008
[14]  
LITHGOW T, 1994, CELL GROWTH DIFFER, V5, P411
[15]   REVERSIBLE MIDDLE CEREBRAL-ARTERY OCCLUSION WITHOUT CRANIECTOMY IN RATS [J].
LONGA, EZ ;
WEINSTEIN, PR ;
CARLSON, S ;
CUMMINS, R .
STROKE, 1989, 20 (01) :84-91
[16]   GLOBAL-ISCHEMIA CAN CAUSE DNA FRAGMENTATION INDICATIVE OF APOPTOSIS IN RAT-BRAIN [J].
MACMANUS, JP ;
BUCHAN, AM ;
HILL, IE ;
RASQUINHA, I ;
PRESTON, E .
NEUROSCIENCE LETTERS, 1993, 164 (1-2) :89-92
[17]   DNA-DAMAGE CONSISTENT WITH APOPTOSIS IN TRANSIENT FOCAL ISCHEMIC NEOCORTEX [J].
MACMANUS, JP ;
HILL, IE ;
HUANG, ZG ;
RASQUINHA, I ;
XUE, D ;
BUCHAN, AM .
NEUROREPORT, 1994, 5 (04) :493-496
[18]  
MERRY DE, 1994, DEVELOPMENT, V120, P301
[19]   CHARACTERIZATION OF MICROGLIAL REACTION AFTER MIDDLE CEREBRAL-ARTERY OCCLUSION IN RAT-BRAIN [J].
MORIOKA, T ;
KALEHUA, AN ;
STREIT, WJ .
JOURNAL OF COMPARATIVE NEUROLOGY, 1993, 327 (01) :123-132
[20]   LOCALIZATION OF 70-KDA STRESS PROTEIN MESSENGER-RNA INDUCTION IN GERBIL BRAIN AFTER ISCHEMIA [J].
NOWAK, TS .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1991, 11 (03) :432-439