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

• Published in: Mediators of inflammation Vol. 2019; no. 2019; pp. 1 - 14
• Main Authors: Qin, Shu, Liu, Tao, Wu, Shiyong, Zhang, Dongying, Chen, Yu, Zhou, Zhenyu, Cai, Guoqiang
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 2019; Hindawi; John Wiley & Sons, Inc; Wiley
• Subjects: Analysis; Apoptosis; Apoptosis - genetics; Apoptosis - physiology; Aprotinin; Arteriosclerosis; Atherosclerosis; Atherosclerosis - genetics; Atherosclerosis - metabolism; Basic Helix-Loop-Helix Transcription Factors - genetics; Basic Helix-Loop-Helix Transcription Factors - metabolism; Bioinformatics; Blotting, Western; Cancer; Cardiovascular disease; Cardiovascular diseases; Cell culture; Cell growth; Cell injury; Cell Proliferation - genetics; Cell Proliferation - physiology; Cell viability; China; Chromosome 5; Coronary vessels; Endothelial cells; Endothelial Cells - metabolism; Endothelium; Enzyme-linked immunosorbent assay; Ethylenediaminetetraacetic acid; Fibroblasts; Flow Cytometry; Genomes; Health aspects; Healthy Volunteers; Human Umbilical Vein Endothelial Cells; Humans; Hypoxia; Inflammation; L-Lactate dehydrogenase; L-Lactate Dehydrogenase - metabolism; Lactic acid; MAP kinase; MicroRNA; MicroRNAs; MicroRNAs - genetics; MicroRNAs - metabolism; miRNA; Monocytes; Mortality; NF-κB protein; Pathogenesis; Penicillin; Physiology; Reactive oxygen species; Reactive Oxygen Species - metabolism; Real-Time Polymerase Chain Reaction; Regulation; Signal transduction; Smooth muscle; Studies; Therapeutic applications; Tumor Necrosis Factor-alpha - metabolism; Tumor necrosis factor-TNF; Tumor necrosis factor-α; China; United States > US
• ISSN: 0962-9351; 1466-1861; 1466-1861
• DOI: 10.1155/2019/1342190

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.