BCL-2 IS EXPRESSED IN NEURONS THAT SURVIVE FOCAL ISCHEMIA IN THE RAT
BCL-2 IS EXPRESSED IN NEURONS THAT SURVIVE FOCAL ISCHEMIA IN THE RAT
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DOI：
10.1097/00001756-199501000-00040
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发表时间：
1995-01-26
期刊：
影响因子：
1.7
通讯作者：
SIMON, RP
中科院分区：
文献类型：
--
作者：
CHEN, J;GRAHAM, SH;SIMON, RP
原癌基因bcl-2的表达在体外可防止程序性细胞死亡，但bcl-2是否在脑缺血后决定细胞存活中起作用尚不清楚。采用免疫组化和Western blot方法，观察大鼠局灶性脑缺血60 min和120 min后24 h脑组织bcl-2蛋白的表达。60分钟的缺血诱导的bcl-2蛋白在整个额顶叶皮层的非梗死区的神经元，而120分钟的缺血诱导的bcl-2的神经元仅在边缘的梗死。bcl-2蛋白在脑梗死边缘区的胶质细胞中也有表达，主要是小胶质细胞。在尾状核和皮质的梗死区域，bcl-2蛋白仅在内皮细胞和血管壁中被诱导。Western blot显示仅在缺血样品中在26 kDa处的特征性单一条带。这些数据表明，bcl-2诱导亚致死损伤的细胞，并建议，bcl-2可以发挥作用，在脑缺血细胞存活的决定。
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.