Junctional adhesion molecule-A-deficient polymorphonuclear cells show reduced diapedesis in peritonitis and heart ischemia-reperfusion injury.

Abstract:

:Junctional Adhesion Molecule-A (JAM-A) is a transmembrane adhesive protein expressed at endothelial junctions and in leukocytes. Here we report that JAM-A is required for the correct infiltration of polymorphonuclear leukocytes (PMN) into an inflamed peritoneum or in the heart upon ischemia-reperfusion injury. The defect was not observed in mice with an endothelium-restricted deficiency of the protein but was still detectable in mice transplanted with bone marrow from JAM-A(-/-) donors. Microscopic examination of mesenteric and heart microvasculature of JAM-A(-/-) mice showed high numbers of PMN adherent on the endothelium or entrapped between endothelial cells and the basement membrane. In vitro, in the absence of JAM-A, PMN adhered more efficiently to endothelial cells and basement membrane proteins, and their polarized movement was strongly reduced. This paper describes a nonredundant role of JAM-A in controlling PMN diapedesis through the vessel wall.

authors

Corada M,Chimenti S,Cera MR,Vinci M,Salio M,Fiordaliso F,De Angelis N,Villa A,Bossi M,Staszewsky LI,Vecchi A,Parazzoli D,Motoike T,Latini R,Dejana E

doi

10.1073/pnas.0500147102

keywords:

subject

Has Abstract

pub_date

2005-07-26 00:00:00

pages

10634-9

issue

30

eissn

0027-8424

issn

1091-6490

pii

0500147102

journal_volume

102

pub_type

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