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physiological angiogenesis.

Most of the data concerning HGF angiogenic activity were obtained from studies on the effects of exogenously administrated HGF. In the physiologic situation, the role of endogenous HGF/c-met system in one or more steps of angiogenic process remains unclear. To contribute to this question we analyzed the expression of the HGF receptor in human umbilical vein endothelial cells (HUVECs) grown in different culture conditions, recapitulating in vitro some steps of angiogenesis. We focused on c-met because previous investigations failed to demonstrate the production of HGF by endothelial cells. Moreover, it is generally accepted that HGF is a mesenchyme-derived factor that acts predominantly on neighboring epithelial and endothelial cells.1

It has been shown earlier that c-met is selectively targeted to the basolateral plasma membrane domain of epithelial cellswhere it is colocalized with E-cadherin at cell-cell adhesion sites.1 The disruption of these sites is accompanied by endocytosis of both E-cadherin and c-met, suggesting that c-met is involved in the regulation of junctional dynamics. To determine whether similar cross-talk occurs between c-met and junctional components of ECs, we compared the expression patterns of c-met with those of vascular endothelial (VE)–cadherin (cadherin-5), an endothelium-specific member of the cadherin family