MicroRNA-34c suppresses proliferation of vascular smooth muscle cell via modulating high mobility group box protein 1

Autor: Xin-Peng Wang, Zhe An, Cui‐Ying Mao, Wen-Qi Zhang, Li-Bo Chen, Rui-Ting Shan, Hai-Kuo Zheng
Rok vydání: 2019
Předmět:
0301 basic medicine
Microbiology (medical)
Vascular smooth muscle
Cell Survival
proliferation
Clinical Biochemistry
Cell
Myocytes
Smooth Muscle
HMGB1
Muscle
Smooth
Vascular
03 medical and health sciences
0302 clinical medicine
Western blot
microRNA
medicine
Immunology and Allergy
Humans
Luciferase
Binding site
HMGB1 Protein
3' Untranslated Regions
Cells
Cultured
Research Articles
Cell Proliferation
biology
medicine.diagnostic_test
Chemistry
Tumor Necrosis Factor-alpha
Biochemistry (medical)
Public Health
Environmental and Occupational Health
NF-kappa B
Hematology
MicroRNA‐34c
Cell biology
high glucose
Medical Laboratory Technology
MicroRNAs
030104 developmental biology
medicine.anatomical_structure
High-mobility group
Glucose
Gene Expression Regulation
high mobility group box protein1
030220 oncology & carcinogenesis
biology.protein
atherosclerosis
vascular smooth muscle cell
Research Article
Zdroj: Journal of Clinical Laboratory Analysis
ISSN: 1098-2825
Popis: Background Atherosclerosis is the most frequent pathological process that causes cardiovascular diseases. Objective The present study aimed to confirm miRNAs associated with atherosclerosis and explore the molecular mechanism of miR-34c and its target high mobility group box protein 1 (HMGB1) in the control of growth of smooth muscle cells in the development of atherosclerosis. Methods Real-time PCR was firstly performed to confirm miRNA correlation with atherosclerosis, and computational analysis and luciferase assay were performed to explore the target of miR-34c, Western blot, and real-time PCR were also utilized to reveal the effect of whether high glucose (HG) and miR-34c affect miR-34c, HMGB1 levels, NF-κB p65 and TNF-α levels, and the role of miR-34c on vascular smooth muscle cells (VSMCs) viability induced by HG. Students' unpaired t test was performed to compare data between two groups. Results MiR-34c level was associated with atherosclerosis with different expression between VSMCs treated with high glucose or normal VSMCs. Then, HMGB1 is a virtual target of miR-34c with predicted binding site resided in HMGB1 3'UTR and further verified by that miR-34c remarkably reduced luciferase activity of wild HMGB1 3'UTR under a concentration-dependent fashion, and miR-34c cannot influence luciferase activity of mutant HMGB1 3'UTR. Conclusions The results suggested miR-34c might be a novel therapeutic strategy in the management of atherosclerosis by suppressing the expression of HGMB1 and its downstream effectors.
Databáze: OpenAIRE
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