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. Author manuscript; available in PMC: 2010 Feb 9.
Published in final edited form as: Circ Res. 2008 Apr 17;102(10):1192–1201. doi: 10.1161/CIRCRESAHA.107.169805

Figure 6. Schematic model of ADAM10-dependent endothelial gap formation.

Figure 6

Thrombin binding to its receptor (PAR-1) induces intracellular signaling pathways, which activate ADAM10-dependent VE-cadherin proteolysis. This effect contributes to endothelial cell dissociation and gap formation. ADAM10 also regulates the transmigration of T cells through the endothelium. Most likely, the binding of activated T cells to the endothelium induces intracellular signaling cascades in endothelial cells, which lead to ADAM10 activation and increased VE-cadherin proteolysis. T cell-expressed ADAM10 might also contribute to the regulation of the transmigration process through cleavage of cell adhesion molecules on the T cell surface or through trans-shedding of endothelial VE-cadherin.