Open AccessmiR‑365b‑3p inhibits the cell proliferation and migration of human coronary artery smooth muscle cells by directly targeting ADAMTS1 in coronary atherosclerosis
Author(s) -
Yue Qu,
Ning Zhang
Publication year - 2018
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2018.6720
Subject(s) - microrna , cancer research , cell growth , vascular smooth muscle , western blot , downregulation and upregulation , transfection , oncogene , cell migration , luciferase , cell , microbiology and biotechnology , biology , cell cycle , cell culture , endocrinology , gene , smooth muscle , biochemistry , genetics
Abnormal proliferation and migration of vascular smooth muscle cells serves a crucial role in the development of atherosclerosis. Previous studies have suggested that some microRNAs (miRs) are involved in this process; however, the associated underlying molecular mechanism is unclear. In present study, human coronary artery smooth muscle cells (HCASMCs) were used to explore the function of miR-365b-3p in the coronary atherosclerosis. It was indicated that platelet-derived growth factor-BB (PDGF-BB) treatment inhibited miR-365b-3p expression and upregulated the expression of a disintegrin and metalloproteinase with thrombospondin motifs 1 (ADAMTS1) in HCASMCs. Subsequently, miR-365b-3p mimic was transfected in HCASMCs to explore the function of this miR. The results of reverse transcription-quantitative polymerase chain reaction and western blot analysis indicated that overexpression of miR-365b-3p significantly downregulated ADAMTS1 expression. Functional assay results revealed that overexpression of miR-365b-3p significantly attenuated PDGF-BB-induced proliferation and migration of HCASMCs. Furthermore, the dual-luciferase reporter assay results confirmed that ADAMTS1 is a direct target gene of miR-365b-3p. This discovery proposed a novel channel of communication between ADAMTS1 and HCASMCs, and suggests a potential therapeutic approach for coronary atherosclerosis.