PuSH - Publication Server of Helmholtz Zentrum München: The junctional adhesion molecule-C promotes neutrophil transendothelial migration in vitro and in vivo.

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Chavakis, T.* ; Keiper, T.* ; Matz-Westphal, R.* ; Hersemeyer, K. ; Sachs, U.J.* ; Nawroth, P.P.* ; Preissner, K.T.* ; Santoso, S.*

The junctional adhesion molecule-C promotes neutrophil transendothelial migration in vitro and in vivo.

J. Biol. Chem. 279, 55602-55608 (2004)

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The third member of the family of junctional adhesion molecules (JAMs), JAM-3, also called JAM-C, was recently shown to be a novel counter-receptor on platelets for the leukocyte beta(2)-integrin Mac-1 (alphaMbeta(2), CD11b/CD18). Here, new functional aspects of the role of endothelial cell JAM-C were investigated. Endothelial cells express JAM-C, which is predominantly localized within junctions at interendothelial contacts, since it codistributes with a tight junction component, zonula occludens-1. Whereas JAM-C does not participate in neutrophil adhesion to endothelial cells, it mediates neutrophil transmigration in a Mac-1-dependent manner. In particular, inhibition of JAM-C significantly reduced neutrophil transendothelial migration, and the combination of JAM-C and platelet/endothelial cell adhesion molecule-1 blockade almost completely abolished neutrophil transendothelial migration in vitro. In vivo, inhibition of JAM-C with soluble mouse JAM-C resulted in a 50% reduction of neutrophil emigration in the mouse model of acute thioglycollate-induced peritonitis. Thus, JAM-C participates in neutrophil transmigration and thereby provides a novel molecular target for antagonizing interactions between vascular cells that promote inflammatory vascular pathologies.

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