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

被引：145

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

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2015年 / 463卷 / 04期

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：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

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

页码：1071 / 1076

页数：6

共 24 条

[1]

[Anonymous], 2010, NATURE, DOI DOI 10.1038/NATURE08938

[2]

[Anonymous], J CLIN EXP OPHTHALMO

[3]

Oxidative stress: A cause and therapeutic target of diabetic complications [J].