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Blood, 15 September 2007, Vol. 110, No. 6, pp. 1848-1856. Prepublished online as a Blood First Edition Paper on May 15, 2007; DOI 10.1182/blood-2006-09-047431. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-09-047431v1 110/6/1848    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Woodfin, A. Articles by Nourshargh, S. Search for Related Content PubMed PubMed Citation Articles by Woodfin, A. Articles by Nourshargh, S. Related Collections Hemostasis, Thrombosis, and Vascular Biology Phagocytes Cell Adhesion and Motility Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY JAM-A mediates neutrophil transmigration in a stimulus-specific manner in vivo: evidence for sequential roles for JAM-A and PECAM-1 in neutrophil transmigration Abigail Woodfin1, Christoph Andreas Reichel2, Andrej Khandoga2, Monica Corada3, Mathieu-Benoit Voisin1, Christoph Scheiermann1, Dorian O. Haskard1, Elisabetta Dejana3, Fritz Krombach2, and Sussan Nourshargh1 1 Cardiovascular Medicine Unit, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, Hammersmith Hospital, London, United Kingdom; 2 Institute for Surgical Research, Ludwig-Maximilians-University of Munich, Munich, Germany; 3 Federazione Italiana per la Ricerca sul Cancro Institute of Molecular Oncology, Department of Biomolecular Sciences and Biotechnologies, University of Milan School of Sciences, Milan, Italy Junctional adhesion molecule-A (JAM-A) is a transmembrane protein expressed at tight junctions of endothelial and epithelial cells and on the surface of platelets and leukocytes. The role of JAM-A in leukocyte transmigration in vivo was directly investigated by intravital microscopy using both a JAM-A–neutralizing monoclonal antibody (mAb) (BV-11) and JAM-A–deficient (knockout [KO]) mice. Leukocyte transmigration (but not adhesion) through mouse cremasteric venules as stimulated by interleukin 1ß (IL-1ß) or ischemia/reperfusion (I/R) injury was significantly reduced in wild-type mice treated with BV-11 and in JAM-A KO animals. In contrast, JAM-A blockade/genetic deletion had no effect on responses elicited by leukotriene B4 (LTB4) or platelet-activating factor (PAF). Furthermore, using a leukocyte transfer method and mice deficient in endothelial-cell JAM-A, evidence was obtained for the involvement of endothelial-cell JAM-A in leukocyte transmigration mediated by IL-1ß. Investigation of the functional relationship between JAM-A and PECAM-1 (CD31) determined that dual blockade/deletion of these proteins does not lead to an inhibitory effect greater than that seen with blockade/deletion of either molecule alone. The latter appeared to be due to the fact that JAM-A and PECAM-1 can act sequentially to mediate leukocyte migration through venular walls in vivo. 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