Junctional adhesion molecule-A-deficient polymorphonuclear cells show reduced diapedesis in peritonitis and heart ischemia-reperfusion injury.
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| 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.
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| Authors | Monica Corada, Stefano Chimenti, Maria Rosaria Cera, Maria Vinci, Monica Salio, Fabio Fiordaliso, Noeleen De Angelis, Antonello Villa, Mario Bossi, Lidia I Staszewsky, Annunciata Vecchi, Dario Parazzoli, Toshiyuki Motoike, Roberto Latini, Elisabetta Dejana |
| Journal | Proceedings of the National Academy of Sciences of the United States of America (Proc Natl Acad Sci U S A) Vol. 102 Issue 30 Pg. 10634-9 (Jul 26 2005) ISSN: 0027-8424 [Print] United States |
| PMID | 16027360 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't) |
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