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ENHANCED SURFACE EXPRESSION OF ASIC2 INHIBITS VSMC MIGRATION
Author(s) -
Grifoni Samira Campos,
Murphy Sydney,
Drummond Heather Anne
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a521-d
Subject(s) - vascular smooth muscle , cell migration , microbiology and biotechnology , small interfering rna , chemistry , platelet derived growth factor receptor , cell , biology , receptor , biochemistry , growth factor , endocrinology , rna , smooth muscle , gene
Vascular smooth muscle cell (VSMC) migration plays a key role in tissue repair after arterial wall injury. Recent studies from our lab demonstrate that A cid S ensing I on C hannel (ASIC) proteins play an important role in VSMC migration. Previous results suggest that at least one ASIC protein, ASIC2, may play an inhibitory role in cell migration. However, it is unknown if enhanced expression of ASIC2 inhibits VSMC migration. Therefore, the aim of the current study was to determine if increased expression of ASIC2 protein at the cell surface inhibits VSMC migration. To address this aim, we enhanced surface expression of ASIC2 using the chemical chaperone glycerol and evaluated P latelet D erived G rowth F actor (PDGF‐bb ‐ 0.05 ng/mL)‐stimulated migration in cultured VSMCs. Using Western blot analysis of surface‐biotinylated proteins, glycerol (500 mM) increased ASIC2 protein expression. In addition, glycerol inhibited PDGF‐stimulated VSMC migration by 41±9.5% (n=6). The inhibitory effect of glycerol on VSMC migration was abolished by silencing ASIC2 expression using small interference RNA (siRNA) approach (n=3). These findings suggest that increased cell surface expression of ASIC2 inhibits VSMC migration. Our data support a novel role for ASIC2 in VSMCs as an inhibitory molecule in VSMC migration. Thus, ASIC2 may act as a negative regulator of vasculogenesis and tissue remodeling. Supported by: NIH‐NHLBI and AHA