Wnt2 and WISP-1/CCN4 Induce Intimal Thickening via Promotion of Smooth Muscle Cell Migration
Author(s) -
Helen Williams,
Carina A.E. Mill,
B.A. Monk,
Sarah L. Hulin-Curtis,
Jason L. Johnson,
Sarah J. George
Publication year - 2016
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.116.307626
Subject(s) - wnt signaling pathway , gene knockdown , vascular smooth muscle , cell migration , intimal hyperplasia , gene silencing , restenosis , small interfering rna , downregulation and upregulation , chemistry , cell , microbiology and biotechnology , medicine , endocrinology , signal transduction , biology , rna , biochemistry , stent , apoptosis , smooth muscle , gene
Increased vascular smooth muscle cell (VSMC) migration leads to intimal thickening which acts as a soil for atherosclersosis, as well as causing coronary artery restenosis after stenting and vein graft failure. Investigating factors involved in VSMC migration may enable us to reduce intimal thickening and improve patient outcomes. In this study, we determined whether Wnt proteins regulate VSMC migration and thereby intimal thickening.
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