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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 (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 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. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted September 15, 2006 Accepted May 8, 2007 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 Woodfin, Christoph Andreas Reichel, Andrej Khandoga, Monica Corada, Mathieu-Benoit Voisin, Christoph Scheiermann, Dorian O Haskard, Elisabetta Dejana, Fritz Krombach, and Sussan Nourshargh* Cardiovascular Medicine Unit, National Heart & Lung Institute, Faculty of Medicine, Imperial College London, Hammersmith Hospital, London, United Kingdom Institute for Surgical Research, Ludwig-Maximilians-University of Munich, Munich, Germany Fondazione Italiana per la Ricerca sul Cancro, Institute of Molecular Oncology, Milan, Italy * Corresponding author; email: s.nourshargh{at}imperial.ac.uk. 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 neutralising mAb (BV-11) and JAM-A deficient (KO) mice. Leukocyte transmigration (but not adhesion) through mouse cremasteric venules as stimulated by IL-1 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 LTB4 or 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-1. 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. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. A. Reichel, M. Rehberg, M. Lerchenberger, N. Berberich, P. Bihari, A. G. Khandoga, S. Zahler, and F. Krombach Ccl2 and Ccl3 Mediate Neutrophil Recruitment via Induction of Protein Synthesis and Generation of Lipid Mediators Arterioscler Thromb Vasc Biol, November 1, 2009; 29(11): 1787 - 1793. [Abstract] [Full Text] [PDF] C. Scheiermann, B. Colom, P. Meda, N. S.A. Patel, M.-B. Voisin, A. Marrelli, A. Woodfin, C. Pitzalis, C. Thiemermann, M. Aurrand-Lions, et al. 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