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

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

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish
Pages (from-to)10634-10639
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume102
Issue number30
DOIs
Publication statusPublished - Jul 26 2005

Keywords

  • Endothelial cell junctions
  • Leukocyte transmigration
  • Myocardial infarction
  • Polymorphonuclear leukocytes

ASJC Scopus subject areas

  • Genetics
  • General

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