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Inhibition of Dll4-mediated signaling induces proliferation of immature vessels and results in poor tissue perfusion.

Inhibition of Dll4-mediated signaling induces proliferation of immature vessels and results in poor tissue perfusion. Research Abstract Details 

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  • Inhibition of Dll4-mediated signaling induces proliferation of immature vessels and results in poor tissue perfusion. Abstract Text:

    jeffrey s scehnetJeffrey S Scehnet,weidong jiangWeidong Jiang,s ram kumarS Ram Kumar,valery krasnoperovValery Krasnoperov,alexandre trindadeAlexandre Trindade,rui beneditoRui Benedito,dusan djokovicDusan Djokovic,cristina borgesCristina Borges,eric j leyEric J Ley,antonio duarteAntonio Duarte,parkash s gillParkash S Gill,

    Vascular development is dependent on various growth factors and certain modifiers critical for providing arterial or venous identity, interaction with the surrounding stroma and tissues, hierarchic network formation, and recruitment of pericytes. Notch receptors and ligands (Jagged and Delta-like) play a critical role in this process in addition to VEGF. Dll4 is one of the Notch ligands that regulates arterial specification and maturation events. In the current study, we have shown that loss of function by either targeted allele deletion or use of a soluble form of Dll4 extracellular domain leads to inhibition of Notch signaling, resulting in increased vascular proliferation but defective maturation. Newly forming vessels have thin caliber, a markedly reduced vessel lumen, markedly reduced pericyte recruitment, and deficient vascular perfusion. sDll4 similarly induced defective vascular response in tumor implants leading to reduced tumor growth. Interference with Dll4-Notch signaling may be particularly desirable in tumors that have highly induced Dll4-Notch pathway.

    Inhibition of Dll4-mediated signaling induces proliferation of immature vessels and results in poor tissue perfusion. Publishing Authors By Initials

    js scehnetJS Scehnet,w jiangW Jiang,sr kumarSR Kumar,v krasnoperovV Krasnoperov,a trindadeA Trindade,r beneditoR Benedito,d djokovicD Djokovic,c borgesC Borges,ej leyEJ Ley,a duarteA Duarte,ps gillPS Gill,

    For similar biological phenomena, cell phenomena, and immunity: cell physiology: cell communication: signal transduction research abstracts see: biological phenomena, cell phenomena, and immunity: cell physiology: cell communication: signal transduction research

    PUBMED ID PMID:

    MEDLINE DATE:

    Inhibition of Dll4-mediated signaling induces proliferation of immature vessels and results in poor tissue perfusion. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Blood

    VOLUME: 109

    Page Numbers: 4753-60

    Journal Abbreviation: Blood

    ISSN: 0006-4971

    DAY: 20

    MONTH: 02

    YEAR: 2007

    Inhibition of Dll4-mediated signaling induces proliferation of immature vessels and results in poor tissue perfusion. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 7603509

    Inhibition of Dll4-mediated signaling induces proliferation of immature vessels and results in poor tissue perfusion. Keywords Mesh Terms:

    KEYWORDS: Signal Transduction

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Inhibition of Dll4-mediated signaling induces proliferation of immature vessels and results in poor tissue perfusion. Information

    Substance Name: Collagen

    Registry Number: 9007-34-5

    Grant and Affiliation Information for Inhibition of Dll4-mediated signaling induces proliferation of immature vessels and results in poor tissue perfusion.

    AFFILIATION: Department of Pathology, Keck School of Medicine, University of Southern California, 1441 Eastlake Avenue, Los Angeles, CA, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NCI

    GRANT: R01 CA 079218-07

    ACRONYM: CA

    MEDLINETA: Blood

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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