MiR-362-3p inhibits the proliferation and migration of vascular smooth muscle cells in atherosclerosis by targeting ADAMTS1
- Department of Clinical Research Center, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016 (China)
- Department of Human Resources, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016 (China)
- Department of Laboratory Medicine, University-Town Hospital of Chongqing Medical University, Chongqing 400016 (China)
Atherosclerosis is a progressive condition of the large arteries that can cause coronary artery disease (CAD). Growing amounts of evidence have indicated that microRNAs (miRNAs, miRs) can be used as diagnostic biomarkers in many cellular processes associated with CAD. MiR-362-3p has been implicated in many biological cellular functions. However, little is known about the role of miR-362-3p during atherosclerosis. In the present study, significant downregulation of miR-362-3p was observed in 110 atherosclerotic CAD patients and not in the 84 controls. The upregulation of miR-362-3p was demonstrated to inhibit vascular smooth muscle cell (VSMC) proliferation and migration, and impede the G1/S cell cycle transition. Bioinformatics analysis indicated that a disintegrin and metalloproteinase with thrombospondin motifs 1 (ADAMTS1) was a direct target of miR-362-3p. Subsequent experiments demonstrated that miR-362-3p binds to the 3′-untranslated region (UTR) of ADAMTS1 and decreases its levels of mRNA and protein expression. Overexpression of ADAMTS1 partially restored the miR-362-3p-mediated inhibition of VSMC proliferation, cell cycle, and migration. Upregulation of ADAMTS1 in plasma samples was detected in atherosclerotic CAD patients. Taken together, our findings suggested that miR-362-3p inhibits the proliferation and migration of VSMCs by directly targeting ADAMTS1, which might provide novel insight into the molecular mechanisms underlying the action of miR-362-3p in atherosclerosis. - Highlights: • MiR-362-3p expression is downregulated in the plasma samples of atherosclerotic CAD patients. • MiR-362-3p overexpression inhibits VSMC proliferation, cell cycle progression, and migration. • ADAMTS1 is a direct target of miR-362-3p. • Dysfunction of miR-362-3p may contribute to the pathophysiology of atherosclerosis.
- OSTI ID:
- 22719124
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 493, Issue 1; Other Information: Copyright (c) 2017 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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