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LncRNA DANCR promotes macrophage lipid accumulation through modulation of membrane cholesterol transporters

Guo-Jun Zhao1, Yu Wang1, Jun-Hong An2

  • 1Affiliated Qingyuan Hospital, Guangzhou Medical University (Qingyuan People’s Hospital), Qingyuan 511518, Guangdong, China.

Aging
|July 5, 2024
PubMed

Insights

Long non-coding RNA DANCR promotes lipid accumulation in macrophages, contributing to atherosclerosis. Inhibiting DANCR reduces lipid droplets and enhances cholesterol efflux, offering a potential therapeutic target for coronary artery disease.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Atherosclerosis Research

Background:

  • Atherosclerosis (AS), a key factor in coronary artery disease (CAD), involves significant lipid deposition in blood vessel walls.
  • Long non-coding RNAs (lncRNAs) are linked to lipid disorders and AS, but the specific role of lncRNA DANCR in atherogenesis is not well understood.

Purpose of the Study:

  • To investigate the role of lncRNA DANCR in macrophage lipid accumulation and its underlying mechanisms in the context of atherosclerosis.
  • To determine if DANCR affects the expression of membrane cholesterol transport proteins and influences cholesterol homeostasis in macrophages.

Main Methods:

  • Quantitative PCR (qPCR) to measure DANCR levels in CAD patients and atherosclerotic mice.
  • In vitro studies using THP-1 and RAW264.7 macrophages treated with ox-LDL to assess DANCR expression and lipid accumulation.
  • Oil Red O staining to quantify lipid droplets; Western blotting and cholesterol efflux assays to evaluate cholesterol transport proteins (ABCA1, ABCG1, SR-BI, CD36, SR-A).
  • Experiments involving DANCR inhibition (siRNA) and overexpression to determine functional effects on lipid uptake and efflux.

Main Results:

  • DANCR expression was significantly higher in CAD patients, atherosclerotic mice, and ox-LDL-treated macrophages.
  • DANCR inhibition reduced lipid droplet accumulation, while DANCR overexpression increased it in macrophages.
  • DANCR modulated the expression of cholesterol transport proteins (ABCA1, ABCG1, SR-BI) and cholesterol efflux.
  • DANCR influenced the uptake of oxidized low-density lipoprotein (ox-LDL) by regulating scavenger receptors (CD36, SR-A).
  • The observed effects of DANCR were independent of miR-33a.

Conclusions:

  • lncRNA DANCR plays a detrimental role in foam cell formation by promoting macrophage lipid accumulation.
  • DANCR regulates macrophage lipid metabolism through its effects on cholesterol transport proteins and LDL uptake.
  • DANCR represents a potential therapeutic target for preventing or treating atherosclerosis.

Keywords:
DANCRcholesterol transportlipid accumulationmacrophagemiR-33a

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