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dc.contributor.authorTakeuchi, Kimioen_US
dc.contributor.authorYanai, Ryojien_US
dc.contributor.authorKumase, Fumiakien_US
dc.contributor.authorMorizane, Yukien_US
dc.contributor.authorSuzuki, Junen_US
dc.contributor.authorKayama, Makien_US
dc.contributor.authorBrodowska, Katarzynaen_US
dc.contributor.authorNakazawa, Mitsuruen_US
dc.contributor.authorMiller, Joan W.en_US
dc.contributor.authorConnor, Kip M.en_US
dc.contributor.authorVavvas, Demetrios G.en_US
dc.date.accessioned2014-04-11T14:12:38Z
dc.date.issued2014en_US
dc.identifier.citationTakeuchi, K., R. Yanai, F. Kumase, Y. Morizane, J. Suzuki, M. Kayama, K. Brodowska, et al. 2014. “EGF-Like-Domain-7 Is Required for VEGF-Induced Akt/ERK Activation and Vascular Tube Formation in an Ex Vivo Angiogenesis Assay.” PLoS ONE 9 (3): e91849. doi:10.1371/journal.pone.0091849. http://dx.doi.org/10.1371/journal.pone.0091849.en
dc.identifier.issn1932-6203en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:12064484
dc.description.abstractEGFL7 is a secreted angiogenic factor, which in contrast to the well-known secreted angiogenic molecules VEGF and FGF-2, is almost exclusively expressed by endothelial cells and may act in an autocrine fashion. Prior studies have shown EGFL7 to mediate its angiogenic effects by interfering with the Notch pathway and/or via the intronic miR126. Less is known about its effects on VEGF signaling. We wanted to investigate the role of epidermal growth factor-like domain 7 (EGFL7) in VEGF-driven angiogenesis using an ex vivo Matrigel-embedded mouse eye cup assay and siRNA mediated knockdown of EGFL7 by siRNA. Our results suggested that VEGF-induced vascular tube formation was significantly impaired after siRNA downregulation of EGFL7. In addition, knockdown of EGFL7 suppressed VEGF upregulation of phospho-Akt and phospho-Erk(1/2) in endothelial cells, but did not alter VEGFR phosphorylation and neuropilin-1 protein expression or miR126 expression. Thus, in conclusion, EGFL7 is required for VEGF upregulation of the Akt/Erk (1/2) pathway during angiogenesis, and may represent a new therapeutic target in diseases of pathological neovascularization.en
dc.language.isoen_USen
dc.publisherPublic Library of Scienceen
dc.relation.isversionofdoi:10.1371/journal.pone.0091849en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3960138/pdf/en
dash.licenseLAAen_US
dc.subjectBiology and life sciencesen
dc.subjectAnatomyen
dc.subjectBiological Tissueen
dc.subjectEpitheliumen
dc.subjectEpithelial Cellsen
dc.subjectEndothelial Cellsen
dc.subjectCell biologyen
dc.subjectSignal transductionen
dc.subjectCell signalingen
dc.subjectSignaling cascadesen
dc.subjectAKT signaling cascadeen
dc.subjectERK signaling cascadeen
dc.subjectExtracellular Matrix Signalingen
dc.subjectMembrane Receptor Signalingen
dc.subjectCellular Typesen
dc.subjectMolecular Cell Biologyen
dc.subjectMedicine and Health Sciencesen
dc.subjectOphthalmologyen
dc.subjectPathology and Laboratory Medicineen
dc.subjectMolecular Pathologyen
dc.subjectVascular Medicineen
dc.subjectVascular Diseasesen
dc.subjectPeripheral Vascular Diseaseen
dc.subjectModel Organismsen
dc.subjectAnimal Modelsen
dc.subjectMouse Modelsen
dc.titleEGF-Like-Domain-7 Is Required for VEGF-Induced Akt/ERK Activation and Vascular Tube Formation in an Ex Vivo Angiogenesis Assayen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalPLoS ONEen
dash.depositing.authorKumase, Fumiakien_US
dc.date.available2014-04-11T14:12:38Z
dc.identifier.doi10.1371/journal.pone.0091849*
dash.authorsorderedfalse
dash.contributor.affiliatedKumase, Fumiaki
dash.contributor.affiliatedConnor, Kip
dash.contributor.affiliatedMiller, Joan
dash.contributor.affiliatedVavvas, Demetrios


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