Abstract：
:Elastin is an essential component of arteries which provides structural integrity and instructs smooth muscle cells to adopt a quiescent state. Despite interaction of endothelial cells with elastin in the internal elastic lamina, the potential for exploiting this interaction therapeutically has not been explored in detail. In this study, we show that tropoelastin (a precursor of elastin) stimulates endothelial cell migration and adhesion more than smooth muscle cells. The biological activity of tropoelastin on endothelial cells is contained in the VGVAPG domain and in the carboxy-terminal 17-amino acids. We show that the effects of the carboxy-terminal 17 amino acids, but not those of VGVAPG, are mediated by integrin α(V)β(3). We demonstrate that tropoelastin covalently linked to stainless steel disks promotes adhesion of endothelial progenitor cells and endothelial cells to the metal surfaces. The adherent cells on the tropoelastin-coated metal surfaces form monolayers that can withstand and respond to arterial shear stress. Because of the unique effects of tropoelastin on endothelial and smooth muscle cells, coating intravascular devices with tropoelastin may stimulate their endothelialization, inhibit smooth muscle hyperplasia, and improve device performance.
journal_name
Ann Biomed Engjournal_title
Annals of biomedical engineeringauthors
Wilson BD,Gibson CC,Sorensen LK,Guilhermier MY,Clinger M,Kelley LL,Shiu YT,Li DYdoi
10.1007/s10439-010-0142-zsubject
Has Abstractpub_date
2011-01-01 00:00:00pages
337-46issue
1eissn
0090-6964issn
1573-9686journal_volume
39pub_type
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