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CCN5 modulates the antiproliferative effect of heparin and regulates cell motility in vascular smooth muscle cells
Authors:Andrew?C?Lake,John?J?Castellot  Suffix"  >Jr  author-information"  >  author-information__contact u-icon-before"  >  mailto:john.castellot@tufts.edu"   title="  john.castellot@tufts.edu"   itemprop="  email"   data-track="  click"   data-track-action="  Email author"   data-track-label="  "  >Email author
Affiliation:(1) Program in Cell, Molecular and Developmental Biology, Sackler School of Biomedical Sciences, Tufts University, 136 Harrison Avenue, Boston, MA 02111, USA;(2) Department of Anatomy and Cell Biology, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111, USA
Abstract:

Background  

Vascular smooth muscle cell (VSMC) hyperplasia plays an important role in both chronic and acute vascular pathologies including atherosclerosis and restenosis. Considerable work has focused on the mechanisms regulating VSMC proliferation and motility. Earlier work in our lab revealed a novel growth arrest-specific (gas) gene induced in VSMC exposed to the antiproliferative agent heparin. This gene is a member of the CCN family and has been given the name CCN5. The objective of the present study is to elucidate the function of CCN5 protein and to explore its mechanism of action in VSMC.
Keywords:
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