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Disordered purinergic signaling inhibits pathological angiogenesis in Cd39/Entpd1-Null mice
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2007 (English)In: American Journal of Pathology, ISSN 0002-9440, E-ISSN 1525-2191, Vol. 171, no 4, 1395-1404 p.Article in journal (Refereed) Published
Abstract [en]

CD39/ecto-nucleoside triphosphate diphosphohydrolase-type-1 (ENTPD1) is the dominant vascular ectonucleotidase that catalyzes the phosphohydrolysis of extracellular nucleotides in the blood and extracellular space. This ecto-enzymatic process modulates endothelial cell, leukocyte, and platelet purinergic receptor-mediated responses to extracellular nucleotides in the setting of thrombosis and vascular inflammation. We show here that deletion of Cd39/Entpd1 results in abrogation of angiogenesis, causing decreased growth of implanted tumors and inhibiting development of pulmonary metastases. Qualitative abnormalities of Cd39-null endothelial cell adhesion and integrin dysfunction were demonstrated in vitro. These changes were associated with decreased activation of focal adhesion kinase and extracellular signaling-regulated kinase-1 and -2 in endothelial cells. Our data indicate novel links between CD39/ENTPD1, extracellular nucleotide-mediated signaling, and vascular endothelial cell integrin function that impact on angiogenesis and tumor growth.

Place, publisher, year, edition, pages
2007. Vol. 171, no 4, 1395-1404 p.
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Medical and Health Sciences
URN: urn:nbn:se:uu:diva-11860DOI: 10.2353/ajpath.2007.070190ISI: 000249969900029PubMedID: 17823293OAI: oai:DiVA.org:uu-11860DiVA: diva2:39629

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Available from: 2008-09-04 Created: 2008-09-04 Last updated: 2013-04-08Bibliographically approved

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Sundberg, Christian
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Department of Medical Biochemistry and Microbiology
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