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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*  

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 were 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 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.

Affiliation:

Central Laboratory, The First Hospital of Hebei Medical University, Shijiazhuang, 050031, Central Laboratory, The First Hospital of Hebei Medical University, Shijiazhuang, 050031, Central Laboratory, The First Hospital of Hebei Medical University, Shijiazhuang, 050031, Central Laboratory, The First Hospital of Hebei Medical University, Shijiazhuang, 050031, Central Laboratory, The First Hospital of Hebei Medical University, Shijiazhuang, 050031, Central Laboratory, The First Hospital of Hebei Medical University, Shijiazhuang, 050031, Hebei International Joint Research Center for Brain Science, Shijiazhuang, 050031, Central Laboratory, The First Hospital of Hebei Medical University, Shijiazhuang, 050031, Central Laboratory, The First Hospital of Hebei Medical University, Shijiazhuang, 050031, Central Laboratory, The First Hospital of Hebei Medical University, Shijiazhuang, 050031



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