Circ_CHMP5 aggravates oxidized low-density lipoprotein-induced damage to human umbilical vein endothelial cells

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Yueru Wang1, Ping Liu2, Xiaoyan Chen3

  • 1Department of Internal Medicine-Cardiovascular, Shanxi Provincial People's Hospital, Taiyuan City, Shanxi, China.

Clinical Hemorheology and Microcirculation
|May 22, 2023
PubMed

Insights

CircRNA-charged multivesicular body protein 5 (circ_CHMP5) exacerbates atherosclerosis by impairing human umbilical vein endothelial cells. Silencing circ_CHMP5 protects against ox-LDL-induced damage via the miR-516b-5p/TGFβR2 pathway, offering potential therapeutic strategies.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Cell Biology

Background:

  • Atherosclerosis (AS) is a leading cause of mortality in the elderly.
  • Endothelial cell dysfunction in human umbilical vein endothelial cells (HUVECs) is implicated in AS pathogenesis.
  • CircRNA-charged multivesicular body protein 5 (circ_CHMP5) has been identified as a potential contributor to AS progression.

Purpose of the Study:

  • To investigate the role of circ_CHMP5 in AS.
  • To elucidate the underlying molecular mechanisms involving miR-516b-5p and transforming growth factor beta receptor 2 (TGFβR2).
  • To evaluate the therapeutic potential of targeting circ_CHMP5 in AS.

Main Methods:

  • Quantitative real-time polymerase chain reaction (qRT-PCR) to measure gene and microRNA expression.
  • Cell proliferation assays (EdU, CCK-8), apoptosis assays (flow cytometry), and tube formation assays.
  • Western blot for protein expression analysis and dual-luciferase reporter/RNA-pull down assays to confirm molecular interactions.

Main Results:

  • Circ_CHMP5 levels were elevated in AS patients and ox-LDL-treated HUVECs.
  • Ox-LDL impaired HUVEC proliferation and angiogenesis while increasing apoptosis; circ_CHMP5 knockdown reversed these effects.
  • Circ_CHMP5 influenced ox-LDL-induced HUVEC dysfunction through the miR-516b-5p/TGFβR2 axis.

Conclusions:

  • Circ_CHMP5 knockdown protects against ox-LDL-induced HUVEC injury by modulating the miR-516b-5p and TGFβR2 pathway.
  • These findings suggest circ_CHMP5 as a novel therapeutic target for AS treatment.
Abstract

Keywords:
ASCirc_CHMP5HUVECsTGFβR2miR-516b-5p

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