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Research Article

视神经粉碎后视网膜神经节细胞凋亡中上调的P53诱导的死亡域蛋白的参与。

卷 20, 期 1, 2020

页: [51 - 59] 页: 9

弟呕挨: 10.2174/1566524019666190918160032

价格: $65

摘要

目的：视网膜神经节细胞（RGCs）凋亡是视神经病变的共同特征。 p53诱导的具有死亡结构域的蛋白（PIDD）是遗传毒性应激诱导的细胞凋亡的众所周知的调节剂，其被组成性切割为三个主要片段：PIDD-N，PIDD-C和PIDD-CC。因此，我们旨在确定PIDD在视神经挤压（ONC）模型中RGC凋亡中的生理相关性。 方法：将所有动物平均随机分为四组：假手术对照组，con-siRNA组，ONC组和PIDD-siRNA组（ONC + PIDD-siRNA）。用Western blot和免疫荧光法分析ONC模型中PIDD，caspase-2，Brn3a和tBid的表达。使用氟金（FG）计算RGC / mm2的平均密度。此外，我们使用TUNEL染色测试了PIDD-siRNA对ONC诱导的RGC凋亡的影响。 结果：全长PIDD的水平较弱，在任何时间点均无显着差异。 ONC后3天，视网膜中的PIDD-CC和PIDD-C显着上调。同时，在Brn3a（RGCs的标记）阳性细胞中，PIDD的表达显着增加，表明PIDD的定位似乎仅限于RGC。此外，抑制PIDD可通过抑制caspase-2和tBid激活来阻止RGC凋亡。 结论：总的来说，PIDD可能在ONC后RGC的凋亡中起关键作用，这一过程可能与caspase-2和tBid有关。

关键词: PIDD，caspase-2，视网膜神经节细胞，凋亡，视神经挤压，RGC。

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