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Updated: Mar 27, 2026
Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
miR-31 Overexpression Exacerbates Atherosclerosis by Targeting NOX4 in apoE(-/-) Mice
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.
Insights
MicroRNA-31 (miR-31) promotes apoptosis in macrophages, a key factor in atherosclerosis. This study reveals miR-31 regulates NOX4, impacting cell viability and migration in atherosclerosis development.
Area of Science:
- Molecular Biology
- Cardiovascular Research
- Cell Biology
Background:
- MicroRNAs (miRNAs) are increasingly recognized for their roles in cellular apoptosis.
- The specific function of miR-31 in the context of atherosclerosis (AS) remains largely unexplored.
- This study investigates the impact of miR-31 on macrophage behavior relevant to AS.
Purpose of the Study:
- To elucidate the role of miR-31 in macrophage apoptosis.
- To determine the relationship between miR-31 and atherosclerosis progression.
- To identify the molecular mechanisms underlying miR-31's effects on macrophages.
Main Methods:
- Quantified miR-31 levels in macrophages from apolipoprotein E knockout (apoE-/-) mice.
- Assessed macrophage cell viability and apoptosis following transfection with miR-31 mimics or inhibitors.
- Investigated the effect of NADPH oxidase 4 (NOX4) knockdown on macrophage apoptosis using siRNA.
Main Results:
- Elevated miR-31 levels were observed in macrophages of apoE-/- mice, correlating with abnormal cell proliferation.
- Overexpression of miR-31 led to decreased cell viability and induced apoptosis in macrophages.
- Knockdown of NOX4 resulted in reduced macrophage migration and increased apoptosis.
Conclusions:
- miR-31 plays a significant role in promoting macrophage apoptosis.
- The observed effects of miR-31 on macrophage apoptosis are mediated through the regulation of NOX4 expression.
