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A circular RNA, circUSP36, accelerates endothelial cell dysfunction in atherosclerosis by adsorbing miR-637 to

Jian-Guo Huang1, Xia Tang1, Jiang-Jie Wang1

  • 1Department of Vascular Surgery, Linyi Central Hospital, Linyi, Shandong Province, China.

Bioengineered
|September 14, 2021
PubMed

Insights

Circular RNA USP36 (circUSP36) exacerbates atherosclerosis by damaging endothelial cells. It sponges miR-637, leading to increased WNT4 expression, promoting cell dysfunction and disease progression.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • RNA Biology

Background:

  • Atherosclerosis is a major global health threat, with circular RNAs (circRNAs) implicated in its pathogenesis.
  • circUSP36 is a key modulator in atherosclerosis, but its precise molecular mechanism remains elusive.

Purpose of the Study:

  • To elucidate the mechanism by which circUSP36 contributes to endothelial cell dysfunction in atherosclerosis.
  • To investigate the role of circUSP36 in response to oxidized low-density lipoprotein (ox-LDL) in vitro.

Main Methods:

  • Confirmed circRNA traits of circUSP36 and assessed its expression in ox-LDL-treated endothelial cells.
  • Performed functional assays (overexpression, depletion) and utilized bioinformatics, luciferase reporter, and RNA pull-down assays.
  • Investigated the circUSP36/miR-637/WNT4 axis in endothelial cell models.

Main Results:

  • circUSP36 expression was upregulated in ox-LDL-treated endothelial cells.
  • Overexpression of circUSP36 inhibited proliferation and migration of these cells.
  • circUSP36 acted as an miRNA sponge for miR-637, and WNT4 was identified as a target of miR-637. Depletion of WNT4 rescued circUSP36-mediated effects.

Conclusions:

  • circUSP36 aggravates ox-LDL-induced endothelial cell injury by sponging miR-637 and regulating WNT4.
  • circUSP36 represents a potential diagnostic biomarker and therapeutic target for atherosclerosis.

Keywords:
AtherosclerosisUSP36Wnt4circRNAendothelial cellmiR-637

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