title: miR-599 Inhibits Vascular Smooth Muscle Cells Proliferation and Migration by Targeting TGFB2.
abstract: Aberrant proliferation and migration of vascular smooth muscle cells (VSMCs) play a crucial role in the pathogenesis of cardiovascular diseases including coronary heart disease, restenosis and atherosclerosis. MicroRNAs are a class of small, non-coding and endogenous RNAs that play critical roles in VSMCs function. In this study, we showed that PDGF-bb, as a stimulant, promoted VSMCs proliferation and suppressed the expression of miR-599. Moreover, overexpression of miR-599 inhibited VSMCs proliferation and also suppressed the PCNA and ki-67 expression. In addition, we demonstrated that ectopic expression of miR-599 repressed the VSMCs migration. We also showed that miR-599 inhibited type I collagen, type V collagen and proteoglycan expression. Furthermore, we identified TGFb2 as a direct target gene of miR-599 in VSMCs. Overexpression of TGFb2 reversed miR-599-induced inhibition of VSMCs proliferation and type I collagen, type V collagen and proteoglycan expression. In conclusion, our findings suggest miR-599 plays a crucial role in controlling VSMCs proliferation and matrix gene expression by regulating TGFb2 expression.
authors.affiliation: Department of Cardiovascular Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
authors.forename: Baodong
authors.initials: B
authors.lastname: Xie
authors.affiliation: Department of Cardiovascular Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
authors.forename: Chunfeng
authors.initials: C
authors.lastname: Zhang
authors.affiliation: Department of Cardiovascular Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
authors.forename: Kai
authors.initials: K
authors.lastname: Kang
authors.affiliation: Department of Cardiovascular Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
authors.forename: Shulin
authors.initials: S
authors.lastname: Jiang
mesh_terms: D050197:Atherosclerosis / Q000235:genetics / Q000473:pathology; D000077214:Becaplermin; D002460:Cell Line; D002465:Cell Movement / Q000235:genetics*; D049109:Cell Proliferation / Q000235:genetics*; D024042:Collagen Type I / Q000096:biosynthesis; D024062:Collagen Type V / Q000096:biosynthesis; D003327:Coronary Disease / Q000235:genetics / Q000473:pathology; D023903:Coronary Restenosis / Q000235:genetics / Q000473:pathology; D006801:Humans; D035683:MicroRNAs / Q000096:biosynthesis / Q000235:genetics*; D009131:Muscle, Smooth, Vascular / Q000166:cytology*; D011509:Proteoglycans / Q000096:biosynthesis; D020574:Proto-Oncogene Proteins c-sis / Q000378:metabolism*; D053781:Transforming Growth Factor beta2 / Q000096:biosynthesis / Q000235:genetics*
chemical_list: D024042:Collagen Type I; D024062:Collagen Type V; C000608803:MIRN599 microRNA, human; D035683:MicroRNAs; D011509:Proteoglycans; D020574:Proto-Oncogene Proteins c-sis; C509041:TGFB2 protein, human; D053781:Transforming Growth Factor beta2; D000077214:Becaplermin