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Circ_0003575 knockdown alleviates ox-LDL-induced human aortic endothelial cell dysfunction in atherosclerosis by

Zhanshuai Zhang1, Shaoqiang Qin1, Rui Wang1

  • 1Department of Cardiovascular Medicine, The First Affiliated Hospital of Hebei North University, Zhangjiakou City, Hebei, China.

Clinical Hemorheology and Microcirculation
|August 21, 2023
PubMed
Abstract

Insights

Circular RNA circ_0003575 promotes atherosclerosis by damaging human aortic endothelial cells. Inhibiting circ_0003575 protects against this damage by regulating the miR-637/TRAF6 and NF-κB pathways.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • RNA Biology

Background:

  • Circular RNAs (circRNAs) are implicated in atherosclerosis (AS) progression.
  • The specific role of circ_0003575 in AS pathogenesis requires elucidation.

Purpose of the Study:

  • To investigate the functional role and underlying mechanism of circ_0003575 in an in vitro model of atherosclerosis.
  • To determine the interaction between circ_0003575, microRNA-637 (miR-637), and TNF receptor associated factor 6 (TRAF6) in endothelial cells.

Main Methods:

  • Established an atherosclerosis cell model using oxidized low-density lipoprotein (ox-LDL) treated human aortic endothelial cells (HAECs).
  • Assessed cell proliferation (CCK-8, EdU), apoptosis (flow cytometry), angiogenesis (tube formation assay), and inflammatory factor release (ELISA).
  • Quantified gene and protein expression (qRT-PCR, Western blot) and investigated molecular interactions (dual-luciferase, RIP assays).

Main Results:

  • Ox-LDL induced endothelial cell injury, characterized by reduced proliferation and angiogenesis, and increased apoptosis and inflammation.
  • Knockdown of circ_0003575 significantly ameliorated ox-LDL-induced HAEC damage.
  • Circ_0003575 directly targeted miR-637, which in turn targeted TRAF6. MiR-637 overexpression mimicked the protective effects of circ_0003575 knockdown.
  • Circ_0003575 silencing inhibited the NF-κB signaling pathway activation.

Conclusions:

  • Circ_0003575 knockdown exerts protective effects against ox-LDL-induced human aortic endothelial cell injury.
  • The mechanism involves the regulation of the miR-637/TRAF6 axis and the NF-κB pathway.
  • Circ_0003575 represents a potential therapeutic target for atherosclerosis.
Keywords:
ASHAECsTRAF6circ_0003575miR-637

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