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          Document History for Document ID 717290

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Document Version Version Comment Date Status
717290.0 [No comment] 06.04.2016 13:46 Released

ID: 717290.0, MPI für molekulare Biomedizin / Jahrbuch 2016 (publ. 2015, arch)
Junctional adhesion molecule B interferes with angiogenic VEGF/VEGFR2 signaling
Authors:Meguenani, M.; Miljkovic-Licina, M.; Fagiani, E.; Ropraz, P.; Hammel, P.; Aurrand-Lions, M.; Adams, R. H.; Christofori, G.; Imhof, B. A.; Garrido-Urbani, S.
Date of Publication (YYYY-MM-DD):2015-08
Title of Journal:FASEB J
Volume:29
Issue / Number:8
Start Page:3411
End Page:3425
Review Status:Internal review
Audience:Not Specified
Abstract / Description:De novo formation of blood vessels is a pivotal mechanism during cancer development. During the past few years, antiangiogenic drugs have been developed to target tumor vasculature. However, because of limitations and adverse effects observed with current therapies, there is a strong need for alternative antiangiogenic strategies. Using specific anti-junctional adhesion molecule (JAM)-B antibodies and Jam-b-deficient mice, we studied the role in antiangiogenesis of JAM-B. We found that antibodies against murine JAM-B, an endothelium-specific adhesion molecule, inhibited microvessel outgrowth from ex vivo aortic rings and in vitro endothelial network formation. In addition, anti-JAM-B antibodies blocked VEGF signaling, an essential pathway for angiogenesis. Moreover, increased aortic ring branching was observed in aortas isolated from Jam-b-deficient animals, suggesting that JAM-B negatively regulates proangiogenic pathways. In mice, JAM-B expression was detected in de novo-formed blood vessels of tumors, but anti-JAM-B antibodies unexpectedly did not reduce tumor growth. Accordingly, JAM-B deficiency in vivo had no impact on blood vessel formation, suggesting that targeting JAM-B in vivo may be offset by other proangiogenic mechanisms. In conclusion, despite the promising effects observed in vitro, targeting JAM-B during tumor progression seems to be inefficient as a stand-alone antiangiogenesis therapy.
Free Keywords:Animals; Cell Adhesion Molecules/*metabolism; Cell Line, Tumor; Female; Mice; Mice, Inbred C57BL; Neovascularization, Pathologic/*metabolism; Signal Transduction/physiology; Vascular Endothelial Growth Factor A/*metabolism; Vascular Endothelial Growth Factor Receptor-2/*metabolism; aortic ring; endothelial cells; tumor angiogenesis
External Publication Status:published
Document Type:Article
Communicated by:Keuker
Affiliations:MPI für molekulare Biomedizin
External Affiliations:*Department of Pathology and Immunology, Medical Faculty, University Medical Center, University of Geneva, Geneva, Switzerland; Department of Biomedicine, Institute of Biochemistry and Genetics, University of Basel, Basel, Switzerland; Unite Mixte de Recherche 1068, Centre de Recherche en Cancerologie de Marseille, Institut National de la Sante et de la Recherche Medicale, Marseille, France; Institut Paoli-Calmettes, Marseille, France; Marseille Universite, Marseille, France; Unite Mixte de Recherche 7258, Centre National de la Recherche Scientifique, Marseille, France; Department of Tissue Morphogenesis, Max-Planck-Institute for Molecular Biomedicine, Munster, Munster, Germany; and Faculty of Medicine, University of Munster, Munster, Germany sarah.garrido-urbani@unige.ch beat.imhof@unige.ch.
Identifiers:ISSN:1530-6860 (Electronic) 0892-6638 (Linking) %R 10.1... [ID No:1]
URL:http://www.ncbi.nlm.nih.gov/pubmed/25911611 [ID No:2]