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A macrophage-specific lncRNA regulates apoptosis and atherosclerosis by tethering HuR in the nucleus

Viorel Simion1, Haoyang Zhou1,2, Stefan Haemmig1

  • 1Department of Medicine, Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.

Nature Communications
|December 2, 2020
PubMed

Insights

A newly discovered long non-coding RNA, MAARS, plays a key role in atherosclerosis by regulating macrophage apoptosis and efferocytosis. Targeting MAARS shows potential for treating vascular diseases.

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • RNA Biology

Background:

  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in disease.
  • Atherosclerosis pathogenesis involves complex cellular and molecular events within the arterial wall.

Purpose of the Study:

  • To identify novel lncRNAs involved in atherosclerosis.
  • To elucidate the function and mechanism of a macrophage-specific lncRNA, MAARS, in atherosclerosis.

Main Methods:

  • RNA sequencing of atherosclerotic lesions.
  • In vivo studies using LDLR-/- mice.
  • In vitro macrophage apoptosis and efferocytosis assays.
  • RNA-binding protein immunoprecipitation and Western blotting.

Main Results:

  • Identified MAARS, a macrophage-specific lncRNA significantly upregulated in atherosclerotic lesions.
  • MAARS knockdown reduced lesion formation by 52% in mice, primarily by decreasing macrophage apoptosis and enhancing efferocytosis.
  • MAARS interacts with HuR/ELAVL1, regulating its cytosolic localization and downstream targets involved in apoptosis (p53, p27, Caspase-9, BCL2).

Conclusions:

  • MAARS is a critical regulator of macrophage apoptosis and efferocytosis in atherosclerosis via HuR.
  • MAARS represents a potential therapeutic target for vascular diseases.

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