title: Wnt3a activates β1-integrin and regulates migration and adhesion of vascular smooth muscle cells.
abstract: Vascular smooth muscle cells (VSMCs) are known to undergo functional changes that contribute to the pathogenesis of atherosclerosis and restenosis. Wnts are a family of secreted glycoproteins that bind to transmembrane Frizzled receptors and initiate signaling cascades with indispensable roles during cell migration, adhesion, proliferation, and survival. The present study reports that wingless-type MMTV integration site family, member 3a (Wnt3a) activates the canonical Wnt pathway in rat VSMCs by triggering the phosphorylation of β-catenin at position Ser675 and GSK-3β at position Ser9. Phosphorylation of these two proteins increases VSMC migration and adhesion. In a search for the downstream mediators of Wnt3a's effects on VSMC migration and adhesion, Wnt3a treatment was observed to increase integrin-linked kinase (ILK) protein expression. ILK is a serine/threonine protein kinase that is thought to control cell migration and adhesion by regulating the affinity of β1-integrin for the extracellular matrix. Wnt3a treatment of VSMCs also activated β1-integrin without changing the quantity of protein expressed on the cell surface. These results demonstrate that Wnt3a enhances migration and adhesion of VSMCs by activating β1-integrin.
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
authors.forename: Xiaolin
authors.initials: X
authors.lastname: Wu
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
authors.forename: Jichun
authors.initials: J
authors.lastname: Wang
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
authors.forename: Hong
authors.initials: H
authors.lastname: Jiang
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
authors.forename: Qi
authors.initials: Q
authors.lastname: Hu
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
authors.forename: Jing
authors.initials: J
authors.lastname: Chen
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
authors.forename: Jing
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of Cardiology, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei 441000, P.R. China.
authors.forename: Rui
authors.initials: R
authors.lastname: Zhu
authors.affiliation: Department of Cardiology, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei 441000, P.R. China.
authors.forename: Wenwei
authors.initials: W
authors.lastname: Liu
authors.affiliation: Department of Cardiology, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei 441000, P.R. China.
authors.forename: Bin
authors.initials: B
authors.lastname: Li
mesh_terms: D000818:Animals; D002448:Cell Adhesion / Q000187:drug effects; D002465:Cell Movement / Q000187:drug effects*; D002478:Cells, Cultured; D024042:Collagen Type I / Q000378:metabolism; D005434:Flow Cytometry; D019012:Integrin beta1 / Q000378:metabolism*; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000166:cytology*; D032389:Myocytes, Smooth Muscle / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D060509:Wnt3A Protein / Q000494:pharmacology*
chemical_list: D024042:Collagen Type I; D019012:Integrin beta1; D060509:Wnt3A Protein