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MicroRNA‐9 inhibits retinal neovascularization in rats with diabetic retinopathy by targeting vascular endothelial growth factor A
Author(s) -
Liu WenLan
Publication year - 2019
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.28081
Subject(s) - vascular endothelial growth factor a , cd31 , retinal , vascular endothelial growth factor , diabetic retinopathy , neovascularization , angiogenesis , apoptosis , microbiology and biotechnology , cancer research , chemistry , biology , endocrinology , biochemistry , vegf receptors , diabetes mellitus
Abstract Diabetic retinopathy (DR) is a leading cause of adult visual impairment and loss. This study aims to explore the effects of microRNA‐9 (miR‐9) on retinal neovascularization during DR by targeting the vascular endothelial growth factor A (VEGFA). DR rat models were successfully established. Retinal microvascular endothelial cells (RMECs) of DR rats were isolated and treated with miR‐9 mimic, miR‐9 inhibitor or small interfering RNA (siRNA)‐VEGFA. The expressions of miR‐9, VEGFA, and cluster of differentiation 31 (CD31) of the rats’ tissues and cells were examined. The targeting relationship between miR‐9 and VEGFA was testified. The tubule formation, the cell proliferation and the periodic distribution and apoptosis were evaluated after transfection. In the retinal tissues of DR rats, miR‐9 expression decreased while the expression of VEGFA and CD31 increased. Notably, miR‐9 targeted and inhibited VEGFA expression. In response to the treatment of miR‐9 mimic and siRNA‐VEGFA, a reduction was identified in CD31 expression, tubule formation, and proliferation of RMECs and cell ratio in the S phase, but an increase was observed in apoptosis rate of RMECs. The treatment of miR‐9 inhibitor reversed the manifestations. Our study demonstrated that miR‐9 could inhibit retinal neovascularization of DR and tubule formation, and promote apoptosis in RMECs by targeting VEGFA.