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Current Pharmaceutical Design


ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

Research Article

Decreased lncRNA SNHG16 Accelerates Oxidative Stress Induced Pathological Angiogenesis in Human Retinal Microvascular Endothelial Cells by Regulating miR-195/mfn2 Axis

Author(s): Rui Zhang, Xiaoying Ma, Lei Jiang , Wenzhen Xia, Haipeng Li, Na Zhao , Ximing Cui, Nan Zhang, Huimin Zhou * and Shunjiang Xu*

Volume 27, Issue 27, 2021

Published on: 02 February, 2021

Page: [3047 - 3060] Pages: 14

DOI: 10.2174/1381612827666210202141541

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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.

Keywords: Oxidative stress, long non-coding RNA, SNHG16, miR-195, Mitofusin 2 (mfn2), endothelial cell.

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