Bcl-2 enhances neurogenesis and inhibits apoptosis of newborn neurons in adult rat brain following a transient middle cerebral artery occlusion
Bcl-2 enhances neurogenesis and inhibits apoptosis of newborn neurons in adult rat brain following a transient middle cerebral artery occlusion
复制标题
DOI：
10.1016/j.nbd.2006.07.012
复制
发表时间：
2006-11-01
影响因子：
6.1
通讯作者：
Sun, Feng-Yan
中科院分区：
文献类型：
--
作者：
Zhang, Rong;Xue, Yu-Yu;Sun, Feng-Yan
为确定Bel-2是否影响成年神经发生和防止新生神经元的凋亡，我们在大鼠大脑中动脉闭塞(MCAO)30min后，立即将Bel-2表达载体注入侧脑室。结果发现，在MCAO后1~4周，Bel-2使同侧纹状体神经前体细胞(BrdU(+)-DCX+)、新生未成熟神经元(BrdU(+)-Tuj-1(+))和新生成熟神经元(BrdU(+)-MAP-2(+))增加。Bcl2过表达促进新生神经元发育为GABA能和胆碱能神经元。此外，通过Tuj-1和激活的caspase-3(Tuj-1(+)-Casp(+))的双重染色，发现Bcl2可显著减少新生神经元的凋亡。这些结果表明，成年大鼠脑内Bcl2的过度表达促进了新生神经元的神经发生和存活。增加神经发生和防止新生神经元死亡可能是帮助中风后成人大脑修复的一种策略。(C)2006 Elsevier Inc.保留所有权利。
To determine whether Bel-2 could influence adult neurogenesis and prevent apoptosis of newborn neurons, we injected Bel-2 expressing plasmid into the lateral ventricle of rat brain immediately following a 30-min occlusion of the middle cerebral artery (MCAO). We found that Bel-2 increased neural progenitor cells (BrdU(+)-DCX+) in the ipsilateral striatum, newborn immature neurons (BrdU(+)-Tuj-1(+)) and newborn mature neurons (BrdU(+)-MAP-2(+)) in the ipsilateral striatum and frontal cortex at 1 to 4 weeks following MCAO. Bcl-2 overexpression promoted development of newborn neurons into GABAergic and cholinergic neurons in the ipsilateral striatum. Moreover, Bcl-2 significantly decreased the apoptosis of newborn neurons, determined by double staining of Tuj-1 and activated caspase-3 (Tuj-1(+)-Casp(+)). These results indicate that overexpression of Bcl-2 in adult rat brain enhances neurogenesis and survival of newborn neurons. Increasing neurogenesis and preventing the death of newborn neuron may be a strategy to aid in the repair of adult brain after stroke. (c) 2006 Elsevier Inc. All rights reserved.