TY - JOUR
T1 - Junctional adhesion molecule-A-deficient polymorphonuclear cells show reduced diapedesis in peritonitis and heart ischemia-reperfusion injury
AU - Corada, Monica
AU - Chimenti, Stefano
AU - Cera, Maria Rosaria
AU - Vinci, Maria
AU - Salio, Monica
AU - Fiordaliso, Fabio
AU - De Angelis, Noeleen
AU - Villa, Antonello
AU - Bossi, Mario
AU - Staszewsky, Lidia I.
AU - Vecchi, Annunciata
AU - Parazzoli, Dario
AU - Motoike, Toshiyuki
AU - Latini, Roberto
AU - Dejana, Elisabetta
PY - 2005/7/26
Y1 - 2005/7/26
N2 - 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.
AB - 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.
KW - Endothelial cell junctions
KW - Leukocyte transmigration
KW - Myocardial infarction
KW - Polymorphonuclear leukocytes
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U2 - 10.1073/pnas.0500147102
DO - 10.1073/pnas.0500147102
M3 - Article
C2 - 16027360
AN - SCOPUS:23044465208
VL - 102
SP - 10634
EP - 10639
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
SN - 0027-8424
IS - 30
ER -