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microRNA‐320a prevent Müller cells from hypoxia injury by targeting aquaporin‐4
Author(s) -
Chen Zhen,
Yang Zhengrong,
Li Xiaoliang,
Wang He,
Wang Yonggang,
Ding Chao,
Yang JingYing,
Ni Ninghua,
Mei Yan,
Zhang Shiwen
Publication year - 2020
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29524
Subject(s) - aquaporin 4 , internalization , hypoxia (environmental) , microbiology and biotechnology , edema , aquaporin 1 , homeostasis , microrna , cell damage , downregulation and upregulation , gene knockdown , cell , medicine , chemistry , biology , pathology , apoptosis , biochemistry , water channel , mechanical engineering , organic chemistry , oxygen , gene , engineering , inlet
Abstract Müller cells are closely related to diabetic retinopathy (DR). Aquaporin‐4 (AQP4) can effectively promote the diffusion of water across cellular membranes. However, the dynamic balance of water plays key role in many diseases, such as cerebral edema. Meanwhile, the unusual expression and distribution of AQP4 in the retina are the significant causes of ocular hypertension and reperfusion injury. To explore the functional significance between microRNA‐320a (miR‐320a) and AQP4 in pathological hypoxia‐induced DR related retinal edema, we hypothesized that miR‐320a regulates AQP4 expression and internalization to relieve the edema of Müller cells under the pathological retinal hypoxia stress by targeting AQP4, thereby attenuate the damage of Müller cells. Results demonstrated that miR‐320a mimics inhibited the expressions of AQP4 in Müller cells. Furthermore, overexpression miR‐320a protected Müller cells by suppressing superoxide anion. In addition, overexpression miR‐320a markedly attenuated hypoxia‐induced injury, significantly increased the cell viability, and promoted the internalization of AQP4. Furthermore, miR‐320a can also regulate the stable anchoring of AQP4 on the cell membrane. Our study indicated that miR‐320a may be a potential modulator which can mediate AQP4 expression and attenuate the hypoxia damage of Müller cells. In conclusion, miR‐320a may be a potential target for DR therapy by targeting AQP4.