Elevation of p-NR2AS1232 by Cdk5/p35 contributes to retinal ganglion cell apoptosis in a rat experimental glaucoma model
Elevation of p-NR2AS1232 by Cdk5/p35 contributes to retinal ganglion cell apoptosis in a rat experimental glaucoma model
复制标题
Cdk5/p35 升高 p-NR2AS1232 导致大鼠实验性青光眼模型中视网膜神经节细胞凋亡
DOI：
10.1016/j.nbd.2011.04.019
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发表时间：
2011-08-01
影响因子：
6.1
通讯作者：
Wang, Zhongfeng
中科院分区：
文献类型：
--
作者：
Chen, Jie;Miao, Yanying;Wang, Zhongfeng
青光眼主要由高眼压（IOP）引起，其特征是视网膜神经节细胞（RGC）的凋亡。我们研究了细胞周期蛋白依赖性激酶 5 (Cdk5) 及其激活剂 p35（与多种神经系统疾病有关）在通过阻断巩膜外静脉复制的大鼠实验性青光眼模型中 RGC 凋亡中的可能参与。霍乱毒素 B 亚基 (CTB) 逆行标记的 RGC 在第 14 天 (D14) 时中央和周边视网膜中的 RGC 数量显着减少 (P
Glaucoma, mainly caused by high intraocular pressure (IOP), is characterized by apoptotic death of retinal ganglion cells (RGCs). We investigated the possible involvement of cyclin-dependent kinase 5 (Cdk5) and its activator p35, which have been implicated in a variety of neurological disorders, in RGC apoptosis in a rat experimental glaucoma model reproduced by blocking episcleral veins. Cholera toxin B subunit (CTB) retrogradely labeled RGCs displayed a dramatic reduction in number both in the central and peripheral retina on day 14 (D14) (P