Affiliation:
1. Central Laboratory, The First Hospital of Hebei Medical University, Shijiazhuang, 050031, China
2. Hebei International Joint Research Center for Brain Science, Shijiazhuang, 050031, China
Abstract
Background:
This study was performed to identify the alterations of Long non-coding RNAs (lncRNAs) induced
by oxidative stress and investigate the functional roles of SNHG16 in the pathological angiogenesis by human retinal
microvascular endothelial cells (HMRECs).
Methods:
The expression profiles of lncRNAs and mRNAs induced by oxidative stress were identified by
RNA-Seq, and the dysregulation of 16 lncRNAs including SNHG16 was verified in H2O2-treated human umbilical
vein endothelial cells (HUVECs). Luciferase reporter assay and RIP analysis were used to investigate the
binding relationship of SNHG16 to miR-195.
Results:
We confirmed that over-expression of SNGH16 attenuated H2O2-induced angiogenesis by HMRECs.
In addition, SNHG16 was significantly decreased, whereas miR-195, a predictive target of SNHG16, was upregulated
in H2O2, HG, and AGE-treated HMRECs. The binding relationship of SNHG16 to miR-195 was subsequently
verified by luciferase reporter assay and RIP analysis. SNHG16 cotransfection abolished miR-195-mediated
repression on mitofusin 2 (mfn2) protein level and counteracted the inductive effect of miR-195 on angiogenesis
by HMRECs.
Conclusion:
These results indicated that decreased SNHG16 accelerates oxidative stress-induced pathological
angiogenesis in HMRECs by regulating the miR-195/mfn2 axis, providing a potential target for diabetic retinopathy
(DR) therapy.
Funder
Health Commission of Hebei Province Program
Science and Technology project of the People's Livelihood in Hebei Province
Hebei Provincial Natural Science Foundation
National Science Foundation of China
Publisher
Bentham Science Publishers Ltd.
Subject
Drug Discovery,Pharmacology
Cited by
17 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献