EXPRESSION OF GLIAL FIBRILLARY ACIDIC PROTEIN (GFAP), GLUTAMINE-SYNTHETASE (GS), AND BCL-2 PROTOONCOGENE PROTEIN BY MULLER (GLIAL) CELLS IN RETINAL LIGHT DAMAGE OF RATS
EXPRESSION OF GLIAL FIBRILLARY ACIDIC PROTEIN (GFAP), GLUTAMINE-SYNTHETASE (GS), AND BCL-2 PROTOONCOGENE PROTEIN BY MULLER (GLIAL) CELLS IN RETINAL LIGHT DAMAGE OF RATS
复制标题
DOI：
10.1016/0304-3940(94)11239-f
复制
发表时间：
1995-02-09
影响因子：
2.5
通讯作者：
REICHENBACH, A
中科院分区：
文献类型：
--
作者：
GROSCHE, J;HARTIG, W;REICHENBACH, A
在视网膜光损伤中，光感受器的变性可引起神经胶质（Muller）细胞的改变。我们进行了免疫细胞化学研究的穆勒细胞从视网膜暴露于增强照明24个月，一个程序，导致感光细胞的完全丧失。一组大鼠在生命的最后8个月内，当剩余的光感受器（约50%）死亡时，每天喂食银杏叶提取物（EGb 761，一种已确定的自由基清除剂）。我们发现（1）Muller细胞通过增加胶质细胞酸性蛋白的表达来响应感光细胞损伤，（2）当主要的谷氨酸释放神经元丢失时，Muller细胞减少谷氨酰胺合成酶的表达，以及（3）外源性自由基清除剂的应用阻止Muller细胞表达原癌基因蛋白Bcl-2，一种被认为能激活内源性自由基清除活性的分子。
In retinal light damage, degeneration of photoreceptors may cause alterations of glial (Muller) cells. We performed immunocytochemical studies on Muller cells isolated from retinae of rats exposed to enhanced illumination for 24 months, a procedure which leads to complete loss of photoreceptor cells. One group of rats was fed daily with Ginkgo biloba extract (EGb 761, an established free radical-scavenger) during the last 8 months of life when the remaining photoreceptors (about 50%) die. We found that (1) Muller cells respond to photoreceptor damage by increased expression of glial fibrillary acidic protein, (2) Muller cells reduce expression of glutamine synthetase when the major glutamate-releasing neurons are lost, and (3) the application of exogenous free radical scavengers prevents the expression by Muller cells of the protooncogene protein Bcl-2, a molecule assumed to activate endogenous free radical-scavenging activities.