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CircRSF1 contributes to endothelial cell growth, migration and tube formation under ox-LDL stress through regulating

Zhenheng Wei1, Huazhong Ran1, Chunhua Yang1

  • 1Department of Cardiovascular Medicine, Zhoukou Central Hospital, Zhoukou, Henan, China.

Life Sciences
|August 14, 2020
PubMed
Abstract

Insights

Circular RNA circRSF1 protects against atherosclerosis by regulating the miR-758/CCND2 pathway, improving endothelial cell function and viability. This suggests circRSF1 as a potential therapeutic target for atherosclerosis treatment.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • RNA Therapeutics

Background:

  • Atherosclerosis involves endothelial cell damage, with circular RNAs (circRNAs) showing therapeutic potential.
  • The specific role of hsa_circ_0000345 (circRSF1) in endothelial dysfunction via competing endogenous RNA (ceRNA) pathways requires investigation.

Purpose of the Study:

  • To investigate the role of circRSF1 in endothelial cell damage within the context of atherosclerosis.
  • To elucidate the mechanism involving circRSF1, microRNA-758-3p (miR-758), and cyclin D2 (CCND2) in a competing endogenous RNA (ceRNA) pathway.

Main Methods:

  • Quantified expression of circRSF1, miR-758, and CCND2 using RT-qPCR and Western blotting.
  • Assessed molecular interactions using dual-luciferase reporter and RNA immunoprecipitation assays.
  • Evaluated endothelial cell viability, migration, tube formation, and apoptosis under oxidized low-density lipoprotein (ox-LDL) conditions.

Main Results:

  • circRSF1 and CCND2 were downregulated, while miR-758 was upregulated in atherosclerosis patients and ox-LDL-treated endothelial cells.
  • circRSF1 restoration and miR-758 silencing improved endothelial cell function and reduced apoptosis.
  • circRSF1 positively regulated CCND2 expression by sponging miR-758, forming a circRSF1/miR-758/CCND2 axis.

Conclusions:

  • circRSF1 protects against ox-LDL-induced endothelial cell injury through the miR-758/CCND2 axis.
  • circRSF1 demonstrates potential as a therapeutic target for atherosclerosis.
Keywords:
AtherosclerosisCCND2HAECsOx-LDLcircRSF1miR-758

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