MicroRNA-30-3p Suppresses Inflammatory Factor-Induced Endothelial Cell Injury by Targeting TCF21

الملخص EN

Atherosclerosis is one of the leading causes of mortality worldwide.

Growing evidence suggested that miRNAs contributed to the progression of atherosclerosis.

miR-30-5p was found involved in various diseases.

However, the role of miR-30-5p in regulation of atherosclerosis is not known.

Here, we aim to investigate the effects of miR-30-5p on regulating the progression of atherosclerosis.

The expression levels of miR-30-5p in serum collected from atherosclerosis patients and normal healthy people were analyzed by qRT-PCR.

Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway bioinformatics were carried out to reveal the possible signaling pathways involved in the mode of action of miR-30-5p.

A potential target gene of miRNA-30-5p was searched and examined by a luciferase reporter assay.

ELISA, Western blot, proliferation, and flow cytometry assays were performed to assess the biological functional role of miR-30-5p in vitro.

Also, an in vitro monocyte-endothelial cell coculture model was used to study the functional role of miR-30-5p in atherosclerosis.

We found that miR-30-5p was significantly decreased in serum samples from atherosclerosis patients compared with control subjects.

GO and KEGG analysis results showed that miR-30-5p is highly associated with genetic profile of cardiovascular disease.

TCF21 was verified as a target gene of miR-30-5p.

Overexpression of miR-30-5p in THP-1 not only protected endothelial cell viability but also inhibited endothelial cell apoptosis, and similar results were observed in cells with that of TCF21 knocked down.

Moreover, miR-30-5p decreased the expression levels of lactate dehydrogenase (LDH) and tumor necrosis factor-α (TNF-α) and reduced reactive oxygen species (ROS) accumulation.

NF-κB and MAPK/p38 pathways played an indispensable role in the protection ability of miR-30-5p against atherosclerosis.

Our results reveal that miR-30-5p suppresses the progression of atherosclerosis through targeting TCF21 in vitro.

Therefore, the miR-30-5p-TCF21-MAPK/p38 signaling pathway may be a potential biomarker or therapeutic target in atherosclerosis.