Inhibition of autophagy induces IL-1β release from ARPE-19 cells via ROS mediated NLRP3 inflammasome activation under high glucose stress

被引:118
作者
Shi, Huanqi [1 ]
Zhang, Zhen [1 ]
Wang, Xiaodan [1 ]
Li, Ruishu [1 ]
Hou, Wenwen [1 ]
Bi, Wenjiao [1 ]
Zhang, Xiaomei [1 ]
机构
[1] Harbin Med Univ, Ophthalmol Hosp, Affiliated Hosp 1, Harbin 150001, Peoples R China
关键词
Diabetic retinopathy; Autophagy; Retinal pigment epithelium; NLRP3; inflammasome;
D O I
10.1016/j.bbrc.2015.06.060
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Autophagy plays an important role in the development of diabetic retinopathy (DR). Retinal pigment epithelial (RPE) cells are the main cells involved in DR, a process in which hyperglycemia plays a crucial role. This study was conducted to investigate the protective effect of autophagy against high glucose-induced inflammatory response in ARPE-19 cells and its underlying mechanism. In the present study we subjected ARPE-19 cells to high glucose stress and showed that ARPE-19 cells respond to high glucose with an increase in autophagy. 3-methyladenine (3-MA) inhibited occurrence of autophagy and it leaded to the accumulation of damaged-mitochondria-producing-ROS, and the activation of NLRP3 inflammasome, and subsequently, caused IL-1 beta secretion. (C) 2015 Elsevier Inc. All rights reserved.
引用
收藏
页码:1071 / 1076
页数:6
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