Long noncoding RNA OIP5-AS1 accelerates the ox-LDL mediated vascular endothelial cells apoptosis through targeting

Minghui Wang1,2, Yujie Liu2, Chao Li2

  • 1Tianjin Medical University Tianjin 300070, China.

Insights

Long noncoding RNA OIP5-AS1 accelerates atherosclerosis by promoting endothelial cell apoptosis. It targets GSK-3β via EZH2, offering potential therapeutic strategies for cardiovascular disease.

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • RNA Biology

Background:

  • Long noncoding RNAs (lncRNAs) are increasingly implicated in cardiovascular diseases like atherosclerosis.
  • The precise mechanism of lncRNA OIP5-AS1 in oxidative low-density lipoprotein (ox-LDL)-induced endothelial cell apoptosis remains largely unknown.

Purpose of the Study:

  • To elucidate the role and mechanism of lncRNA OIP5-AS1 in ox-LDL-mediated endothelial cell apoptosis.
  • To investigate the interaction between OIP5-AS1, EZH2, and GSK-3β in the context of atherosclerosis.

Main Methods:

  • Quantitative analysis of OIP5-AS1 expression in ox-LDL treated human umbilical vein endothelial cells (HUVECs).
  • OIP5-AS1 silencing experiments to assess effects on apoptosis and cell cycle.
  • Chromatin immunoprecipitation (ChIP) assays to determine the recruitment of EZH2 to the GSK-3β promoter.
  • Rescue experiments to validate the role of GSK-3β.

Main Results:

  • OIP5-AS1 was significantly over-expressed in ox-LDL treated HUVECs.
  • Silencing OIP5-AS1 inhibited apoptosis and promoted proliferation by inducing G0/G1 cell cycle arrest.
  • OIP5-AS1 recruits EZH2 to the GSK-3β promoter, leading to reduced GSK-3β expression.
  • GSK-3β was found to counteract the effects of OIP5-AS1.

Conclusions:

  • lncRNA OIP5-AS1 accelerates ox-LDL-mediated vascular endothelial cell apoptosis by targeting GSK-3β through EZH2 recruitment.
  • These findings highlight OIP5-AS1 as a potential therapeutic target for atherosclerosis.
  • The OIP5-AS1/EZH2/GSK-3β axis represents a novel pathway in endothelial cell apoptosis regulation.

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