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Published on: June 15, 2018
microRNA-181a is upregulated in human atherosclerosis plaques and involves in the oxidative stress-induced
1Department of Internal Medicine, Tianjin Huanhu Hospital, Hexi District, Tianjin, China. gangliuhhh@163.com.
Insights
MicroRNA 181a (miR-181a) is upregulated in atherosclerosis and worsens endothelial dysfunction by targeting Bcl-2. Inhibiting miR-181a restores Bcl-2, increasing resistance to oxidative stress.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Biochemistry
Background:
- Atherosclerosis involves artery wall thickening due to inflammatory cell infiltration and smooth muscle cell proliferation.
- Endothelial dysfunction is a key factor in various vascular diseases, including atherosclerosis.
- MicroRNAs (miRNAs) are implicated in the pathogenesis of atherosclerotic plaque formation.
Purpose of the Study:
- To investigate the role of miR-181a in oxidative stress-induced endothelial cell dysfunction.
- To explore the relationship between miR-181a and Bcl-2 in the context of atherosclerosis.
Main Methods:
- Compared miR-181a expression in human atherosclerotic plaques versus normal vessels.
- Quantified Bcl-2 protein and mRNA levels using Western blot and qRT-PCR.
- Overexpressed miR-181a in human umbilical vein endothelial cells (HUVECs) and assessed cell viability under hydrogen peroxide (H2O2) exposure using MTT assay.
Main Results:
- miR-181a expression was significantly higher in atherosclerotic plaques and induced by H2O2.
- Overexpression of miR-181a increased HUVEC apoptosis in response to H2O2.
- Bcl-2 was identified as a direct target of miR-181a; H2O2 inhibited Bcl-2 expression.
- miR-181a inhibition restored Bcl-2 expression and enhanced H2O2 resistance.
- A negative correlation between miR-181a and Bcl-2 was observed in human atherosclerotic plaques.
Conclusions:
- miR-181a plays a critical role in atherosclerosis development by regulating endothelial dysfunction.
- The miR-181a/Bcl-2 pathway is a potential therapeutic target for atherosclerosis treatment.
- Findings provide mechanistic insights for developing novel antioxidant therapies for atherosclerosis.
Objective:
Atherosclerosis is featured as artery wall thickness as a result of invasion and accumulation of white blood cells and proliferation of intimal smooth muscle cells. Endothelial dysfunction has been linked to a variety of vascular diseases, including atherosclerosis. MicroRNAs play essential roles during the atherosclerotic plaques formation. In this study, we investigate the roles of miR-181a in the oxidative stress-induced endothelial cells dysfunction.
Materials And Methods:
The expressions of miR-181a were compared between human atherosclerotic plaques and normal blood vessels. The Bcl-2 protein expression was measured by Western blot and mRNA expression was measured by qRT-PCR. HUVECs were transiently transfected with pre-miR-181a or control microRNAs by Lipofectamine 2000. The viability of HUVECs in response to H2O2 was measured by MTT assay.
Results:
We report miR-181a is upregulated in human atherosclerotic plaques compared with the normal blood vessel. The miR-181a is induced by H2O2 treatments. The exogenous overexpression of miR-181a accelerates the apoptosis rates of HUVECs in response to H2O2. We identify Bcl-2 as a direct target of miR-181a. Also, we observed H2O2 treatments inhibited Bcl-2 expressions at both protein and mRNA levels. Inhibition of miR-181a restores Bcl-2 expressions, leading to increased resistance to H2O2. Moreover, restoration of Bcl-2 in miR-181a-overexpressing HUVECs renders cells tolerate higher concentrations of H2O2. Finally, a reverse correlation between miR-181a and Bcl-2 expression in human atherosclerosis plaques is illustrated.
Conclusions:
Our results revealed an essential role of miR-181a in the development of atherosclerosis through the regulation of the endothelial dysfunction, providing mechanisms for the development of new antioxidant drugs for the treatment of atherosclerosis.
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