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Blood, 15 July 2005, Vol. 106, No. 2, pp. 725-733.
Prepublished online as a Blood First Edition Paper on April 12, 2005; DOI 10.1182/blood-2004-11-4416.
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PHAGOCYTES
Junctional adhesion molecule-A deficiency increases hepatic ischemia-reperfusion injury despite reduction of neutrophil transendothelial migration
Andrej Khandoga,
Julia S. Kessler,
Herbert Meissner,
Marc Hanschen,
Monica Corada,
Toshiyuki Motoike,
Georg Enders,
Elisabetta Dejana, and
Fritz Krombach
From the Institute for Surgical Research and the Institute of Pathology, Ludwig-Maximilians-University of Munich, Munich, Germany; the Department of Vascular Biology, Italian Foundation for Cancer Research Institute of Molecular Oncology, Milan, Italy; Department of Biomolecular and Biotechnological Sciences, Faculty of Sciences, University of Milan, Milan, Italy; and The University of Texas Southwestern Medical Center at Dallas, Dallas, TX.
The endothelial receptors that control leukocyte transmigration in the postischemic liver are not identified. We investigated the role of junctional adhesion molecule-A (JAM-A), a receptor expressed in endothelial tight junctions, leukocytes, and platelets, for leukocyte transmigration during hepatic ischemia-reperfusion (I/R) in vivo. We show that JAM-A is up-regulated in hepatic venular endothelium during reperfusion. I/R-induced neutrophil transmigration was attenuated in both JAM-A-/- and endothelial JAM-A-/- mice as well as in mice treated with an anti-JAM-A antibody, whereas transmigration of T cells was JAM-A independent. Postischemic leukocyte rolling remained unaffected in JAM-A-/- and endothelial JAM-A-/- mice, whereas intravascular leukocyte adherence was increased. The extent of interactions of JAM-A-/- platelets with the postischemic endothelium was comparable with that of JAM-A+/+ platelets. The I/R-induced increase in the activity of alanine aminotransferase (ALT)/aspartate aminotransferase (AST) and sinusoidal perfusion failure was not reduced in JAM-A-/- mice, while the number of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling (TUNEL)-positive hepatocytes was significantly higher. Thus, we show for the first time that JAM-A is up-regulated in hepatic venules and serves as an endothelial receptor of neutrophil transmigration, but it does not mediate leukocyte rolling, adhesion, or platelet-endothelial cell interactions. JAM-A deficiency does not reduce I/R-induced microvascular and hepatocellular necrotic injury, but increases hepatocyte apoptosis, despite attenuation of neutrophil infiltration. (Blood. 2005;106:725-733)
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