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Melatonin inhibits Müller cell activation and pro‐inflammatory cytokine production via upregulating the MEG3/miR‐204/Sirt1 axis in experimental diabetic retinopathy
Author(s) -
Tu Yuanyuan,
Zhu Manhui,
Wang Zhenzhen,
Wang Kun,
Chen Lili,
Liu Wangrui,
Shi Qin,
Zhao Qingliang,
Sun Yake,
Wang Xiaoyu,
Song E.,
Liu Xiaojuan
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29716
Subject(s) - melatonin , luzindole , cytokine , endocrinology , sirtuin 1 , downregulation and upregulation , gliosis , medicine , diabetic retinopathy , meg3 , chemistry , diabetes mellitus , pathology , melatonin receptor , long non coding rna , biochemistry , gene
Diabetic retinopathy (DR) is the most common ocular complication caused by diabetes mellitus and is the main cause of visual impairment in working‐age people. Reactive gliosis and pro‐inflammatory cytokine production by Müller cells contribute to the progression of DR. Melatonin is a strong anti‐inflammatory hormone, mediating the cytoprotective effect of a variety of retinal cells against hyperglycemia. In this study, melatonin inhibited the gliosis activation and inflammatory cytokine production of Müller cells in both in vitro and in vivo models of DR. The melatonin membrane blocker, Luzindole, invalidated the melatonin‐mediated protective effect on Müller cells. Furthermore, melatonin inhibited Müller cell activation and pro‐inflammatory cytokine production by upregulating the long noncoding RNA maternally expressed gene 3/miR‐204/sirtuin 1 axis. In conclusion, our study suggested that melatonin treatment could be a novel therapeutic strategy for DR.