Details

Autor(en) / Beteiligte

• Zhang, Rui
• Ma, Xiaoying
• Jiang, Lei
• Xia, Wenzhen
• Li, Haipeng
• Zhao, Na
• Cui, Ximing
• Zhang, Nan
• Zhou, Huimin
• Xu, Shunjiang

Titel

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

Ist Teil von

• Current pharmaceutical design, 2021-01, Vol.27 (27), p.3047-3060

Ort / Verlag

United Arab Emirates

Erscheinungsjahr

2021

Quelle

MEDLINE

Beschreibungen/Notizen

• 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). 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 H O -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. We confirmed that over-expression of SNGH16 attenuated H O -induced angiogenesis by HMRECs. In addition, SNHG16 was significantly decreased, whereas miR-195, a predictive target of SNHG16, was upregulated in H O ;, 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. 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.