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

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

Volume: 27 Issue: 27

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

Affiliation:

• Central Laboratory, The First Hospital of Hebei Medical University, Shijiazhuang, 050031,China

• Central Laboratory, The First Hospital of Hebei Medical University, Shijiazhuang, 050031,China

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

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.

Cite this article as:

Zhang Rui , Ma Xiaoying, Jiang Lei , Xia Wenzhen , Li Haipeng, Zhao Na , Cui Ximing, Zhang Nan, Zhou Huimin*, Xu Shunjiang *, Decreased lncRNA SNHG16 Accelerates Oxidative Stress Induced Pathological Angiogenesis in Human Retinal Microvascular Endothelial Cells by Regulating miR-195/mfn2 Axis, Current Pharmaceutical Design 2021; 27 (27) . https://dx.doi.org/10.2174/1381612827666210202141541