Dataset Information

Up-regulation of miR-203 expression induces endothelial inflammatory response: Potential role in preeclampsia.

ABSTRACT:

Problem

To determine whether miR-203 mediates endothelial inflammatory response in preeclampsia.

Method of study

Maternal vessel miR-203 expression was assessed by in situ hybridization. Suppressor of cytokine signaling-3 (SOCS-3) and ICAM expression was determined by immunostaining. Subcutaneous fat tissue sections from normal and preeclamptic pregnant women were used. miR-203-induced inflammatory response was evaluated by the measurements of IL-6, IL-8, ICAM, and VCAM expression and production and neutrophil adhesion in the endothelial cells (EC) transfected with miR-203 precursor, pre-miR-203. SOCS3 expression was also determined.

Results

Up-regulation of miR-203 and ICAM expression and down-regulation of SOCS-3 expression were demonstrated in maternal vessel endothelium in preeclampsia. Overexpression of miR-203 resulted in down-regulation of SOCS-3 expression and increases in the production of IL-6, IL-8, ICAM, and VCAM and neutrophil adhesion in ECs.

Conclusion

As miR-203 is an inflammatory microRNA, increased miR-203 production/expression in ECs could diminish an anti-inflammatory activity and increase the endothelial inflammatory response in preeclampsia.

SUBMITTER: Wang Y

PROVIDER: S-EPMC5118090 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature

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Publications

Up-regulation of miR-203 expression induces endothelial inflammatory response: Potential role in preeclampsia.

Wang Yuping Y Dong Qin Q Gu Yang Y Groome Lynn J LJ

American journal of reproductive immunology (New York, N.Y. : 1989) 20161018 6

<h4>Problem</h4>To determine whether miR-203 mediates endothelial inflammatory response in preeclampsia.<h4>Method of study</h4>Maternal vessel miR-203 expression was assessed by in situ hybridization. Suppressor of cytokine signaling-3 (SOCS-3) and ICAM expression was determined by immunostaining. Subcutaneous fat tissue sections from normal and preeclamptic pregnant women were used. miR-203-induced inflammatory response was evaluated by the measurements of IL-6, IL-8, ICAM, and VCAM expression ...[more]

PMID: 27753461

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Project description:Atherosclerosis is the leading cause of death from vascular diseases worldwide, and endothelial cell (EC) dysfunction is the key cause of atherosclerosis. miR-155 was found to induce endothelial injury and to trigger atherosclerosis. In addition, brain and muscle ARNT-like protein-1 (Bmal1) has been found to be closely related to EC function. Therefore, the present study aimed to explore the mechanism underlying the regulation of Bmal1 by miR-155 in the induction of EC apoptosis and inflammatory response in atherosclerosis. The atherosclerosis model in apolipoprotein E (ApoE)- / - mice was established. miR-155 and Bmal1 expression was quantified by RT-qPCR and western blot analysis, respectively. The role of miR-155 and Bmal1 in atherosclerosis was evaluated through changes in cardiac function, plaque area, cardiomyocyte apoptosis, and inflammatory factor levels in mice. Moreover, the regulatory relationship between them was identified by dual-luciferase reporter gene assay to explore the mechanism of action of miR-155. After the modeling, the expression of miR-155 was upregulated and Bmal1 was downregulated in aorta, and there was a significant linear correlation between them. Upregulation of miR-155 increased the atherosclerotic plaque area, cell apoptosis, total cholesterol (TC) and triglyceride (TG), as well as weakened aortic diastolic function. However, opposite changes occurred after downregulation of miR-155 or an increase in Bmal1. In addition, the microRNA.org website predicted that there were targeted binding sites between miR-155 and Bmal1, which was verified with a dual-luciferase reporter gene assay. miR-155 was able to inhibit the expression by targeting Bmal1. Moreover, a rescue experiment showed that Bmal1 hindered the promotion of miR-155 in regards to atherosclerosis. In conclusion, miR-155 induces EC apoptosis and inflammatory response, weakens aortic diastolic function, and promotes the progression of atherosclerosis through targeted inhibition of Bmal1.

Dataset Information

Up-regulation of miR-203 expression induces endothelial inflammatory response: Potential role in preeclampsia.

Problem

Method of study

Results

Conclusion

Publications

Up-regulation of miR-203 expression induces endothelial inflammatory response: Potential role in preeclampsia.

Similar Datasets

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