title: Vasostatin-2 inhibits cell proliferation and adhesion in vascular smooth muscle cells, which are associated with the progression of atherosclerosis.
abstract: Recently, the serum expression level of vasostatin-2 was found to be reduced and is being studied as an important indicator to assess the presence and severity of coronary artery disease; the functional properties of vasostatin-2 and its relationship with the development of atherosclerosis remains unclear. In this study, we attempted to detect the expression of vasostatin-2 and its impact on human vascular smooth muscle cells (VSMCs). Quantitative real-time PCR (qRT-PCR) and western blot were used to assess the expression level of vasostatin-2 in VSMCs between those from atherosclerosis and disease-free donors; we found that vasostatin-2 was significantly down-regulated in atherosclerosis patient tissues and cell lines. In addition, the over-expression of vasostatin-2 apparently inhibits cell proliferation and migration in VSMCs. Gain-of-function in vitro experiments further show that vasostatin-2 over-expression significantly inhibits inflammatory cytokines release in VSMCs. In addition, cell adhesion experimental analysis showed that soluble adhesion molecules (sICAM-1, sVCAM-1) had decreased expression when vasostatin-2 was over-expressed in VSMCs. Therefore, our results indicate that vasostatin-2 is an atherosclerosis-related factor that can inhibit cell proliferation, inflammatory response and cell adhesion in VSMCs. Taken together, our results indicate that vasostatin-2 could serve as a potential diagnostic biomarker and therapeutic option for human atherosclerosis in the near future.
authors.affiliation: Department of Cardiovascular, Weinan Center Hospital, The Middle of Victory Avenue, Linwei District, Weinan City 714000, China. Electronic address: jianghonghou@163.com.
authors.forename: Jianghong
authors.initials: J
authors.lastname: Hou
authors.affiliation: Department of Cardiovascular, The First Affiliated Hospital, College of Medicine, Xi'an Jiaotong University, Xi'an 710061, China.
authors.forename: Xiaolin
authors.initials: X
authors.lastname: Xue
authors.affiliation: Department of Cardiovascular, Weinan Center Hospital, The Middle of Victory Avenue, Linwei District, Weinan City 714000, China.
authors.forename: Junnong
authors.initials: J
authors.lastname: Li
mesh_terms: D050197:Atherosclerosis / Q000378:metabolism* / Q000473:pathology; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D049109:Cell Proliferation; D002478:Cells, Cultured; D053379:Chromogranin A / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000473:pathology / Q000503:physiopathology*; D032389:Myocytes, Smooth Muscle / Q000378:metabolism* / Q000473:pathology; D010446:Peptide Fragments / Q000378:metabolism*
chemical_list: D015815:Cell Adhesion Molecules; D053379:Chromogranin A; D010446:Peptide Fragments; C102106:vasostatin II
keywords: Atherosclerosis; Inflammation; Proliferation; VSMCs; Vasostatin-2