Role of MEG3 in Cellular Physiology of Atherosclerosis

Yu-Ting Wu1, Zhi-Jun Guo1, Jiang-Bin Li2

  • 1Department of Geriatrics, Quanzhou First Hospital, Quanzhou, Fujian, China.

Abstract

Insights

Long non-coding RNA MEG3 (MEG3) is downregulated in atherosclerosis (AS). Overexpressing MEG3 reduces lipid accumulation and enhances cholesterol efflux, suggesting it acts as an anti-atherosclerotic factor via the miR-200b-3p/ABCA1 pathway.

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Genetics

Background:

  • Atherosclerosis (AS) involves complex biochemical processes.
  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in disease pathogenesis.

Purpose of the Study:

  • To investigate the role of lncRNA MEG3 in counteracting the biochemical mechanisms underlying atherosclerosis development.
  • To elucidate the molecular pathway involving MEG3, miR-200b-3p, and ABCA1 in AS.

Main Methods:

  • Expression analysis of MEG3, miR-200b-3p, and ABCA1 in AS patients and healthy controls using RT-qPCR.
  • Assessment of lipid accumulation and cholesterol efflux in macrophage-derived foam cells.
  • Dual luciferase assays to determine targeting relationships between MEG3, miR-200b-3p, and ABCA1.

Main Results:

  • MEG3 and ABCA1 expression were decreased, while miR-200b-3p was upregulated in AS patients.
  • Overexpression of MEG3 in foam cells reduced lipid accumulation and increased cholesterol efflux.
  • MEG3 overexpression led to decreased miR-200b-3p and increased ABCA1 expression, with partial reversal by co-expressed miR-200b-3p.

Conclusions:

  • MEG3 expression is reduced in atherosclerosis and foam cells.
  • Upregulated MEG3 exhibits anti-atherosclerotic effects by modulating lipid accumulation and cholesterol efflux.
  • The miR-200b-3p/ABCA1 axis is a key mediator of MEG3's protective function in AS.

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