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Molecular Biologic study for ischemic damage to retinal ganglion cells.

视网膜神经节细胞缺血性损伤的分子生物学研究。

基本信息

批准号：
08672036
负责人：
KITANO Shigehiko
金额：
$ 1.41万
依托单位：
Tokyo Women's Medical College
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1996
资助国家：
日本
起止时间：
1996 至 1998
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-08672036/
关键词：
Retinal ganglion cell Excitatory amino acid Ischemia Heat shock protein Muller cell

项目摘要

Knowledge of the mechanisms by which retinal ganglion cells are damaged may provide information required to develop novel treatments for diseases that cause retinal ganglion cell death. The authors investigated whether the expression of the 72-kDa heat shock protein in cultured rat retinal ganglion cells increases tolerance to hypoxic and excitotoxic injury.Hyperthermia (42* far 1 hour) and sublethal hypoxia (10% 02 for 6 hours) were used to induce synthesis of the 72-kDa heat shock protein in cultured rat retinal ganglion cells and cultured retinal Muller cells. Induction of the 72.kDa heat shock protein was detected with immunocytochemical and immunoblot techniques. Survival of cultured retinal ganglion cells after exposure to anoxia (0% 02 for 6 hours) and glutamate (200 mum 6or 6 hours) was measured and compared to control cultures stressed previously by hyperthermia or sublethal hypoxia. The effect of quercetin, a blocker of heat shock protein synthesis, was evaluated in parallel … More experiments.Heat shock protein immunoreactivity was expressed in cultured retinal ganglion cells and Muller cell after hyperthermia and sublethal hypoxia. The mean (* standard deviation) retinal ganglion cell survival rates after exposure to anoxia (expressed as a percentage of untreated control cultures) in cells pretreated with sublethal hypoxia (83% * 17%) and hyperthermia (82% * 19%) were significantly greater than for cells that had no pretreatment (50% * 18%, P <0.001). The mean (* standard deviation) retinal ganglion cell survival rate after exposure to glutamate in cells pretreated with sublethal hypoxia (82% * 19%) and hypcrthermia (86% * 17%) were significantly greater than for ceus that had no pretreatment (56% * 17%, P <0.001). Inhibition of heat shock protein synthesis with quercetin abolished the protective effects of sublethal hypoxia and hyperthermia on cell survival after anoxia and glutamate exposure.The neuroprotective effect of hyperthermia and sublethal hypoxia suggests that heat shock proteins confer protection against ischemic and excitotoxic retinal ganglion cell death. Less

了解视网膜神经节细胞受损的机制可能为开发导致视网膜神经节细胞死亡的疾病的新治疗方法提供所需的信息。作者研究了72kda热休克蛋白在培养的大鼠视网膜神经节细胞中的表达是否增加了对缺氧和兴奋毒性损伤的耐受性。采用高温（42*远1小时）和亚致死缺氧（10% 02低氧6小时）诱导培养的大鼠视网膜神经节细胞和培养的视网膜Muller细胞合成72-kDa热休克蛋白。72的归纳。采用免疫细胞化学和免疫印迹技术检测kDa热休克蛋白。测定培养的视网膜神经节细胞暴露于缺氧（0% o2 6小时）和谷氨酸（200 mum 6或6小时）后的存活情况，并与先前通过高温或亚致死缺氧应激的对照培养物进行比较。槲皮素是一种热休克蛋白合成阻滞剂，对其效果进行了平行评价。热休克蛋白免疫反应性在体外培养的视网膜神经节细胞和Muller细胞中表达。经亚致死缺氧（83% * 17%）和热疗（82% * 19%）预处理的细胞暴露于缺氧后的视网膜神经节细胞存活率（以未处理对照培养物的百分比表示）显著高于未预处理的细胞（50% * 18%,P <0.001）。经亚致死缺氧（82% * 19%）和低温（86% * 17%）预处理的视网膜神经节细胞暴露于谷氨酸后的平均（*标准差）存活率显著高于未经预处理的ceus （56% * 17%, P <0.001）。槲皮素抑制热休克蛋白合成可消除亚致死缺氧和高热对缺氧和谷氨酸暴露后细胞存活的保护作用。高温和亚致死缺氧的神经保护作用表明，热休克蛋白对缺血性和兴奋性毒性视网膜神经节细胞死亡具有保护作用。少