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Am J Physiol Heart Circ Physiol (December 13, 2001). doi:10.1152/ajpheart.00921.2001
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Articles in PresS, published online ahead of print December 13, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00921.2001
Submitted on October 24, 2001
Accepted on December 7, 2001

Del1 mediates vascular smooth muscle cell adhesion, migration and proliferation through interaction with integrin avb3

Mehrdad Rezaee1, Penta Kalyani1, and Quertermous Thomas1*

1 Donald W. Reynolds Cardiovascular Research Center, Stanford University, Stanford, CA, USA

* To whom correspondence should be addressed. E-mail: tomq1{at}stanford.edu.

Del1 is a matrix protein transiently expressed by embryonic endothelial cells. It was recently demonstrated that vascular endothelial cells adhere and interact with Del1 through {alpha}vß3 integrins, providing an autocrine angiogenic signaling pathway in this cell type. To determine whether Del1 might signal to other cell types in the vessel wall in a paracrine fashion, studies were conducted with vascular smooth muscle cells (VSMC). Del1 promoted adhesion and migration of VSMC in a dose dependent fashion. These functions were mediated through {alpha}vß3 integrins, as the vitronectin receptor inhibitory peptide PCN-GRGDSP and an antibody specific for the {alpha}vß3 integrin specifically blocked both adhesion and migration. Adhesion of VSMC to Del1 was associated with organization of actin filaments and formation of focal contacts enriched in vinculin and {alpha}vß3 . Furthermore, Del1 supported VSMC proliferation, at least in part by inhibiting these cells from undergoing apoptosis. These data, in conjunction with evidence that Del1 expression is reactivated in vascular injury, suggest that Del1 may have a paracrine role in vessel wall development and remodeling.




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