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Circ_0026218 ameliorates oxidized low-density lipoprotein-induced vascular endothelial cell dysfunction by regulating

Jing Liu1, Xiangyang Zhang2, Zhaoxia Yu3

  • 1Departments of coronary heart disease, First Affiliated Hospital of Xinjiang Medical University, Urumqi City, China.

Cardiovascular Drugs and Therapy
|December 30, 2022
PubMed

Insights

Knocking down circular RNA circ_0026218 alleviates atherosclerosis by regulating the microRNA-188-3p/toll-like receptor 4/NF-κB pathway in human umbilical vein endothelial cells.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • RNA Biology

Background:

  • Circular RNAs (circRNAs) are implicated in cardiovascular diseases like atherosclerosis (AS).
  • The specific role and mechanism of circ_0026218 in AS pathogenesis remain largely unknown.
  • Understanding circRNA regulation is crucial for developing novel therapeutic strategies for AS.

Purpose of the Study:

  • To investigate the function and mechanism of circ_0026218 in atherosclerosis.
  • To determine the regulatory relationship between circ_0026218, microRNA-188-3p (miR-188-3p), and toll-like receptor 4 (TLR4) in endothelial cells.
  • To explore the potential of circ_0026218 as a therapeutic target for AS.

Main Methods:

  • Established an in vitro cell model of AS using oxidized low-density lipoprotein (ox-LDL)-treated human umbilical vein endothelial cells (HUVECs).
  • Quantified expression levels of circ_0026218, miR-188-3p, and TLR4 in patient serum and cell models using RT-qPCR.
  • Assessed cell proliferation, apoptosis, inflammation, oxidative stress, and nitric oxide production using various assays (CCK-8, EdU, flow cytometry, ELISA, NO assay).
  • Investigated molecular interactions using dual-luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays.
  • Analyzed exosome characteristics and presence using transmission electron microscopy (TEM) and nanoparticle tracking analysis (NTA).

Main Results:

  • Ox-LDL induced HUVEC dysfunction, characterized by inhibited proliferation, increased apoptosis, inflammation, and oxidative stress.
  • Circ_0026218 expression was significantly upregulated in AS patient serum and ox-LDL-treated HUVECs.
  • Knockdown of circ_0026218 ameliorated ox-LDL-induced HUVEC dysfunction.
  • Circ_0026218 sponged miR-188-3p, and miR-188-3p targeted TLR4, collectively regulating the TLR4/NF-κB pathway.
  • Circ_0026218 was found to be packaged and transferred via exosomes.

Conclusions:

  • Circ_0026218 plays a critical role in promoting endothelial cell dysfunction in atherosclerosis.
  • The circ_0026218/miR-188-3p/TLR4/NF-κB axis represents a key regulatory pathway in AS pathogenesis.
  • Circ_0026218, particularly when delivered via exosomes, is a potential therapeutic target for atherosclerosis.
Abstract

Keywords:
NF-κBTLR4atherosclerosiscirc_0026218exosomemiR-188-3p

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