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Growth arrest‐specific gene 6 expression in proliferating rabbit vascular smooth muscle cells in vitro and in vivo
Author(s) -
Yin Jianlin,
McLachlan Craig,
Chaufour Xavier,
McGuire Mark A.,
White Geoffrey,
Turner Virginia,
King Nicholas J. C.,
Hambly Brett D.
Publication year - 2000
Publication title -
electrophoresis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.666
H-Index - 158
eISSN - 1522-2683
pISSN - 0173-0835
DOI - 10.1002/1522-2683(200011)21:17<3851::aid-elps3851>3.0.co;2-q
Subject(s) - vascular smooth muscle , platelet derived growth factor receptor , restenosis , gas6 , microbiology and biotechnology , thrombin , biology , growth factor , platelet derived growth factor , cell growth , receptor tyrosine kinase , receptor , cancer research , kinase , platelet , endocrinology , medicine , immunology , smooth muscle , biochemistry , stent
Proliferation and migration of vascular smooth muscle cells (VSMCs) are involved in the processes of atherosclerosis and restenosis. The protein product of the growth arrest‐specific gene 6 (Gas‐6) has recently been identified as a ligand for the Axl/Rse/Mer tyrosine kinase receptor family, which may be involved in proliferation and migration of VSMCs. Here we show that Gas‐6 gene expression is increased in proliferating VSMCs in tissue culture (2.5‐fold increase by Northern blot) and following neointimal proliferation in a rabbit balloon‐injury model (3‐fold increase by Western blot). Neither platelet‐derived growth factor (PDGF) nor thrombin stimulate the expression of Gas‐6 in cultured VSMCs despite the ability of the PDGF, but not thrombin, to stimulate proliferation in growth‐arrested cells. These data suggest a role for the Gas‐6 regulatory system in VSMC proliferation, which may be a target for therapeutic interventions in the atherosclerotic process and restenosis after angioplasty.