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