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Blocking circ_UBR4 suppressed proliferation, migration, and cell cycle progression of human vascular smooth muscle

Ying Zhang1, Cheng Zhang1, Zongwei Chen1

  • 1Department of Cardiology, Zhongshan Affiliated Hospital, Dalian University, No. 6, Zhonshan Road, Dalian, 116001, Liaoning, China.

Open Life Sciences
|May 13, 2021
PubMed

Insights

Circular RNA UB R4 (circ_UBR4) promotes atherosclerosis by increasing vascular smooth muscle cell proliferation and migration via the circ_UBR4/miR-107/ROCK1 pathway.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Cell Biology

Background:

  • Atherosclerosis (AS) involves vascular smooth muscle cell (VSMC) dysfunction.
  • Oxidized low-density lipoprotein (ox-LDL) contributes to AS pathogenesis.
  • The role of circ_UBR4 in ox-LDL-induced VSMC dysfunction is unclear.

Purpose of the Study:

  • To investigate the role of circ_UBR4 in ox-LDL-induced VSMC proliferation and migration.
  • To elucidate the regulatory pathway involving circ_UBR4, miR-107, and Rho-associated coiled-coil containing kinase 1 (ROCK1).

Main Methods:

  • Expression analysis of circ_UBR4, miR-107, and ROCK1 in AS models.
  • Functional assays following circ_UBR4 knockdown in VSMCs.
  • Investigation of the circ_UBR4/miR-107/ROCK1 interaction.

Main Results:

  • circ_UBR4 and ROCK1 were upregulated, while miR-107 was downregulated in AS.
  • circ_UBR4 depletion inhibited VSMC proliferation, viability, and migration.
  • ROCK1 upregulation counteracted the effects of circ_UBR4 knockdown, mediated by miR-107 targeting.

Conclusions:

  • circ_UBR4 promotes VSMC proliferation and migration in an ox-LDL-induced AS model.
  • The circ_UBR4/miR-107/ROCK1 axis is a key pathway in AS pathogenesis.
  • circ_UBR4 represents a potential therapeutic target for atherosclerosis.

Keywords:
ROCK1VSMCsatherosclerosiscirc_UBR4miR-107

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