自噬
生物
细胞生物学
细胞凋亡
视网膜
神经退行性变
溶酶体
程序性细胞死亡
细胞内
生物化学
内科学
医学
酶
疾病
作者
Li Wang,Xiaodong Sun,Manhui Zhu,Jingxia Du,Jiaowen Xu,Xiao Qin,Xun Xu,E Song
标识
DOI:10.1016/j.yexcr.2019.04.014
摘要
Retinal neurodegeneration is an early feature in the pathogenesis of diabetic retinopathy (DR). Autophagy is an intracellular catabolic process involved in protein and organelle degradation that has been linked in DR. Epigallocatechin gallate (EGCG) is a major polyphenol in green tea that has beneficial effects in diabetic. however, it is not currently known whether EGCG can regulate Müller cell autophagy. Here, we showed that EGCG increased autophagy by promoting the formation of autophagosomes, increasing lysosomal acidification, and stimulating autophagic flux in Müller cells, while high glucose (HG) induced a decrease in autophagy and an increase in apoptosis. However, retinal Müller cells in HG treated with EGCG showed autophagy machinery activation and reestablishment of cargo degradation, protecting the cells from apoptosis. EGCG could increase the ability of cells to proliferate by increasing autophagy. In an experimental model of diabetic retinopathy, EGCG reduced the reactive gliosis of Müller cells and decreased retinal damage. These results highlight that HG downregulates autophagy and accumulates P62 cargo due to lysosomal dysfunction and then increases apoptosis, which was reversed by treatment with EGCG. This finding might be valuable for developing a novel therapeutic strategy to treat DR.
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