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Galectin‐1 Modulates Focal Adhesion Turnover and Migration of Vascular Smooth Muscle Cells
Author(s) -
Chau LeeYoung,
Chiang MingTsai,
Tsai DongLin,
Tsai MinShao
Publication year - 2017
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.31.1_supplement.931.2
Subject(s) - focal adhesion , vascular smooth muscle , microbiology and biotechnology , fibronectin , extracellular matrix , vinculin , cell migration , chemistry , phosphorylation , biology , cell , biochemistry , endocrinology , smooth muscle
Background Vascular smooth muscle cell (VSMC) migration play a key role in the development of atherosclerosis and restenosis. Galectin‐1 (Gal‐1) is a galactose‐binding lectin highly expressed in VSMCs. Previous studies have shown that Gal‐1 binds to extracellular matrix and β1integrin. Whether Gal‐1 influences VSMC motility via regulating focal adhesion dynamics remains to be characterized. Methods and Results The motilities of primary VSMCs isolated from wild type (WT) and Gal‐1 null mice were assessed by wound healing and Boyden chamber assays. Gal‐1 null VSMCs were shown to exhibit greater motility than WT cells. Moreover, recombinant Gal‐1 (0.5~2 μg/ml) inhibited the migration of Gal‐1 null VSMCs in a dose‐dependent manner. On the other hand, adhesion assay revealed that WT VSMCs adhered better than Gal‐1 null cells on surfaces coated with matrix proteins, including fibronectin, laminin and collagen. Cell spreading and focal adhesion formation examined by phalloidin and vinculin staining following plating on fibronectin were significantly greater in WT SMCs. Concomitantly, FAK phosphorylation examined by Western blot analysis was induced to greater extent in WT cells. Nocodazole washout assay demonstrated that focal adhesion disassembly was facilitated in Gal‐1 null VSMCs, which was correlated with faster decrease in FAK phosphorylation in these cells. In line with the in vitro findings, the neointimal hyperplasia induced by carotid artery ligation was much greater in Gal‐1 null mice comparing to WT control. Conclusion These data demonstrate that Gal‐1 restricts neointimal formation post vascular injury at least in part through attenuating focal adhesion turnover in VSMCs. Support or Funding Information This work was supported by a grant from the Ministry of Science and Technology of Taiwan (MOST‐103‐2321‐B‐001‐071)