LncRNA KCNQ1OT1 depletion inhibits the malignant development of atherosclerosis by miR-145-5p

Microvasc Res. 2022 Jan:139:104236. doi: 10.1016/j.mvr.2021.104236. Epub 2021 Aug 28.

Abstract

Background: Atherosclerosis (AS) is a lipid-driven inflammatory disease of the arterial intima. Evidence is growing that dysregulation of lncRNAs is implicated in the pathogenesis of AS. In this research, the role of lncRNA KCNQ1OT1 in AS was investigated.

Methods: ApoE-/- mice were fed on a high fat diet to establish mouse models of AS. Macrophages (THP-1) were treated with oxidized low-density lipoprotein (ox-LDL) to establish cell models of AS. Atherosclerotic lesions of AS mice were determined by performing Oil red O staining. Lipid metabolic disorders and inflammatory were detected using specific assay kits. KCNQ1OT1 and miR-145-5p expression was measured using RT-qPCR. Levels of PPARα and CPT1 were measured using western blot.

Results: KCNQ1OT1 expression was upregulated and miR-145-5p was downregulated in atherosclerotic plaques of AS mice and ox-LDL-treated THP-1 cells. Lipid metabolic disorders and inflammation in vivo and in vitro were attenuated by either KCNQ1OT1 knockdown or miR-145-5p overexpression. Additionally, KCNQ1OT1 acted as a molecular sponge of miR-145-5p and downregulated miR-145-5p expression. Furthermore, silencing miR-145-5p abolished the effect of KCNQ1OT1 knockdown.

Conclusion: Silencing KCNQ1OT1 attenuates AS progression by sponging miR-145-5p.

Keywords: Atherosclerosis; KCNQ1OT1; Ox-LDL; miR-145-5p.

MeSH terms

  • Animals
  • Aorta* / drug effects
  • Aorta* / metabolism
  • Aorta* / pathology
  • Aortic Diseases* / genetics
  • Aortic Diseases* / metabolism
  • Aortic Diseases* / pathology
  • Aortic Diseases* / prevention & control
  • Atherosclerosis* / genetics
  • Atherosclerosis* / metabolism
  • Atherosclerosis* / pathology
  • Atherosclerosis* / prevention & control
  • Disease Models, Animal
  • Disease Progression
  • Gene Expression Regulation
  • Humans
  • Inflammation* / genetics
  • Inflammation* / metabolism
  • Inflammation* / pathology
  • Inflammation* / prevention & control
  • Lipoproteins, LDL / toxicity
  • Macrophages* / drug effects
  • Macrophages* / metabolism
  • Macrophages* / pathology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout, ApoE
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • Plaque, Atherosclerotic
  • Potassium Channels, Voltage-Gated / genetics
  • Potassium Channels, Voltage-Gated / metabolism
  • RNA Interference
  • RNA, Long Noncoding* / genetics
  • RNA, Long Noncoding* / metabolism
  • Signal Transduction
  • THP-1 Cells

Substances

  • KCNQ1OT1 long non-coding RNA, human
  • Lipoproteins, LDL
  • MicroRNAs
  • MIRN145 microRNA, human
  • MIRN145a microRNA, mouse
  • oxidized low density lipoprotein
  • Potassium Channels, Voltage-Gated
  • RNA, Long Noncoding
  • KCNQ1OT1 RNA