miR-125a-3p aggravates ox-LDL-induced HUVEC injury through BAMBI

Feng Xia1, Qingrong Zeng1

  • 1Department of Cardiovascular Surgery, Wuhan Asia General Hospital, Wuhan, Hubei, China.

Insights

MicroRNA-125a-3p (miR-125a-3p) exacerbates vascular dysfunction in atherosclerosis by targeting BAMBI. This microRNA promotes cell damage and apoptosis in human umbilical vein endothelial cells (HUVECs) treated with oxidized low-density lipoprotein (ox-LDL).

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Cellular Pathology

Background:

  • Atherosclerosis (AS) is a chronic inflammatory arterial disease.
  • MicroRNAs (miRNAs) are key regulators of lipoprotein homeostasis and plaque formation in AS.
  • The specific role of microRNA-125a-3p (miR-125a-3p) in AS pathogenesis is currently unknown.

Purpose of the Study:

  • To investigate the role and mechanism of miR-125a-3p in the pathogenesis of atherosclerosis.
  • To examine the effect of miR-125a-3p on human umbilical vein endothelial cells (HUVECs) under oxidized low-density lipoprotein (ox-LDL) stimulation.

Main Methods:

  • Established an in vitro AS model using HUVECs treated with ox-LDL.
  • Quantified miR-125a-3p and BAMBI expression using qRT-PCR and Western blot.
  • Assessed HUVEC viability, apoptosis, and the miR-125a-3p/BAMBI interaction via CCK-8, TUNEL, flow cytometry, and dual-luciferase assays.

Main Results:

  • miR-125a-3p expression was significantly upregulated in ox-LDL-treated HUVECs.
  • miR-125a-3p potentiated ox-LDL-induced reduction in HUVEC viability and increased apoptosis.
  • BAMBI was identified as a direct target of miR-125a-3p, and its overexpression counteracted miR-125a-3p's effects.

Conclusions:

  • miR-125a-3p aggravates ox-LDL-induced HUVEC dysfunction by targeting BAMBI.
  • miR-125a-3p plays a significant role in the pathogenesis of atherosclerosis.
  • Targeting miR-125a-3p may offer a therapeutic strategy for AS.