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Conserved miR-370-3p/BMP-7 axis regulates the phenotypic change of human vascular smooth muscle cells

Title
Conserved miR-370-3p/BMP-7 axis regulates the phenotypic change of human vascular smooth muscle cells
Authors
Kim, YerinYu, NamheeJang, Ye EunLee, EunkyungJung, YeonjooLee, Doo JaeTaylor, W. RobertJo, HanjoongKim, JaesangLee, SanghyukKang, Sang Won
Ewha Authors
이상혁강상원김재상이두재정연주
SCOPUS Author ID
이상혁scopus; 강상원scopus; 김재상scopus; 이두재scopus; 정연주scopus
Issue Date
2023
Journal Title
SCIENTIFIC REPORTS
ISSN
2045-2322JCR Link
Citation
SCIENTIFIC REPORTS vol. 13, no. 1
Publisher
NATURE PORTFOLIO
Indexed
SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
Endothelial dysfunction and inflammatory immune response trigger dedifferentiation of vascular smooth muscle cells (SMCs) from contractile to synthetic phenotype and initiate arterial occlusion. However, the complex vascular remodeling process playing roles in arterial occlusion initiation is largely unknown. We performed bulk sequencing of small and messenger RNAs in a rodent arterial injury model. Bioinformatic data analyses reveal that six miRNAs are overexpressed in injured rat carotids as well as synthetic-type human vascular SMCs. In vitro cell-based assays show that four miRNAs (miR-130b-5p, miR-132-3p, miR-370-3p, and miR-410-3p) distinctly regulate the proliferation of and monocyte adhesion to the vascular SMCs. Individual inhibition of the four selected miRNAs strongly prevents the neointimal hyperplasia in the injured rat carotid arteries. Mechanistically, miR-132-3p and miR-370-3p direct the cell cycle progression, triggering SMC proliferation. Gene ontology analysis of mRNA sequencing data consistently reveal that the miRNA targets include gene clusters that direct proliferation, differentiation, and inflammation. Notably, bone morphogenic protein (BMP)-7 is a prominent target gene of miR-370-3p, and it regulates vascular SMC proliferation in cellular and animal models. Overall, this study first reports that the miR-370-3p/BMP-7 axis determines the vascular SMC phenotype in both rodent and human systems.
DOI
10.1038/s41598-022-26711-z
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자연과학대학 > 생명과학전공 > Journal papers
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