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The neuroprotective roles of Muller cell in rat retinal ischemia-reperfusion injury

Muller细胞对大鼠视网膜缺血再灌注损伤的神经保护作用

基本信息

批准号：
18591911
负责人：
ARAI Jun
金额：
$ 2.57万
依托单位：
Shinshu University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2006
资助国家：
日本
起止时间：
2006 至 2007
项目状态：
已结题

项目摘要

Purpose: We presented that the heat-shock proteins were expressed in Muller cells after rat retinal ischemia-reperfusion injury. To investigate the neuroprotective roles of Muller cells played in rat retinal ischemia-reperfusion injury by using the crystallin family short interfering RNA (siRNA).Methods: Retinal ischemia for 60 minutes was induced in rats by increasing the intraocular pressure to 110 mm Hg. The expression of 13E32-crystallin in the retina was determined by Western blot, real-time polymerase chain reaction (PCR), and immunohistochemistry. To inhibit the upregulation of βB2-crystallin, intravitreal injection of βB2-crystallin siRNA was performed before ischemia. The inhibition of Bβ2-crystallin expression was studied on Western blotting.Results: The expression of 6132-crystallin mRNA and protein were up-regulated at 6 hours after reperfusion and peaked at 12 hours. The βB2-crystallin immunoreactivities were detected in ganglion cells at 12 hours after reperfusion. The βB2-crystallin expression in the retina treated with siRNA of (βB2-crystallin was reduced at 12 hours after reperfusion compared with that injected with the control siRNA. On Western blotting, βB2-crystallin was downregulated at 12 hours after reperfusion. On TUNEL methods, the number of TUNEL positive cells in the ganglion cell layer and the internal nuclear layer reduced at 12 hours after ischemia-reperfusion injury. Conversely, αB-crystallin induced in Muller cell.Conclusions: pB2-crystallin may regulate the retinal ganglion cell death after ischemia-reperfusion injury. On the other hand, Muller cell might protect the ischemic retinal injuries due to αB-crystallin.

目的：研究大鼠视网膜缺血再灌注损伤后热休克蛋白在Muller细胞中的表达。目的：用晶体蛋白家族短干扰RNA(SiRNA)研究Muller细胞在大鼠视网膜缺血再灌注损伤中的神经保护作用。方法：将眼压升高至110 mm Hg，诱导大鼠视网膜缺血60min。用Western印迹、实时聚合酶链式反应和免疫组织化学方法检测视网膜中13E32-晶状体蛋白的表达。为抑制βB2-晶状体蛋白表达上调，在缺血前玻璃体内注射βB2-晶状体蛋白小干扰RNA。结果：Bβ2晶状体蛋白的表达在再灌流6h开始上调，12h达高峰。再灌注12h神经节细胞内检测到βB2-晶状体蛋白免疫反应阳性。再灌注12h后，经βB2-晶体蛋白干扰RNA处理的视网膜中βB2-晶体蛋白的表达较对照组明显减少。Western blotting显示，再灌注12h后，βB2-晶体蛋白表达下调。原位末端标记法显示，缺血再灌注后12h，神经节细胞层和内核层的TUNEL阳性细胞数减少。结论：α-晶状体蛋白可能参与调控视网膜神经节细胞在缺血再灌注损伤后的死亡。另一方面，米勒细胞可能对αB晶状体蛋白所致的视网膜缺血性损伤具有保护作用。