miR-31 Overexpression Exacerbates Atherosclerosis by Targeting NOX4 in apoE(-/-) Mice

Clin Lab. 2015;61(11):1617-24. doi: 10.7754/clin.lab.2015.150322.

Abstract

Background: Increasing evidence has shown that microRNAs are involved in apoptosis in different cells. However, the role of miR-31 in atherosclerosis (AS) has never been elucidated. In the present study, we identified the impact of miR-31 on atherosclerosis in macrophages.

Methods: The level of miR-31 in macrophages was examined in apoE-/- mice. Cell viability and apoptosis were examined in macrophage cells transfected with miR-31 mimics, inhibitors or negative control. In addition, the impact of NOX4 on cell apoptosis was tested with a specific siRNA targeting NADPH oxidase 4 (NOX4).

Results: An enhanced level of miR-31 was found in macrophage cells of apoE-/- mice, suggesting that miR-31 might contribute to abnormal cell proliferation of macrophage cells. Upregulation of miR-31 decreased cell viability and induced macrophage cell apoptosis. Moreover, knockdown of NOX4 reduced cell migration capacity and enhanced cell apoptosis.

Conclusions: The current data suggested that miR-31 contributed to macrophage apoptosis by regulating the expression of NOX4.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apolipoproteins E / genetics
  • Apolipoproteins E / physiology*
  • Apoptosis
  • Atherosclerosis / genetics
  • Atherosclerosis / pathology*
  • Lipoproteins, LDL / blood
  • Macrophages / pathology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • MicroRNAs / genetics*
  • NADPH Oxidase 4
  • NADPH Oxidases / genetics*

Substances

  • Apolipoproteins E
  • Lipoproteins, LDL
  • MicroRNAs
  • Mirn31 microRNA, mouse
  • NADPH Oxidase 4
  • NADPH Oxidases
  • Nox4 protein, mouse