Please use this identifier to cite or link to this item: https://doi.org/10.1074/jbc.M113.544833
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dc.titleSemaphorin 3d and Semaphorin 3e Direct Endothelial Motility through Distinct Molecular Signaling Pathways
dc.contributor.authorAghajanian, Haig
dc.contributor.authorChoi, Connie
dc.contributor.authorHo, Vivienne C
dc.contributor.authorGupta, Mudit
dc.contributor.authorSingh, Manvendra K
dc.contributor.authorEpstein, Jonathan A
dc.date.accessioned2021-09-27T09:03:52Z
dc.date.available2021-09-27T09:03:52Z
dc.date.issued2014-06-27
dc.identifier.citationAghajanian, Haig, Choi, Connie, Ho, Vivienne C, Gupta, Mudit, Singh, Manvendra K, Epstein, Jonathan A (2014-06-27). Semaphorin 3d and Semaphorin 3e Direct Endothelial Motility through Distinct Molecular Signaling Pathways. JOURNAL OF BIOLOGICAL CHEMISTRY 289 (26) : 17971-17979. ScholarBank@NUS Repository. https://doi.org/10.1074/jbc.M113.544833
dc.identifier.issn00219258
dc.identifier.issn1083351X
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/201189
dc.description.abstractClass 3 semaphorins were initially described as axonal growth cone guidance molecules that signal through plexin and neuropilin coreceptors and since then have been established to be regulators of vascular development. Semaphorin 3e (Sema3e) has been shown previously to repel endothelial cells and is the only class 3 semaphorin known to be capable of signaling via a plexin receptor without a neuropilin coreceptor. Sema3e signals through plexin D1 (Plxnd1) to regulate vascular patterning by modulating the cytoskeleton and focal adhesion structures. We showed recently that semaphorin 3d (Sema3d) mediates endothelial cell repulsion and pulmonary vein patterning during embryogenesis. Here we show that Sema3d and Sema3e affect human umbilical vein endothelial cells similarly but through distinct molecular signaling pathways. Time-lapse imaging studies show that both Sema3d and Sema3e can inhibit cell motility and migration, and tube formation assays indicate that both can impede tubulogenesis. Endothelial cells incubated with either Sema3d or Sema3e demonstrate a loss of actin stress fibers and focal adhesions. However, the addition of neuropilin 1 (Nrp1)-blocking antibody or siRNA knockdown of Nrp1 inhibits Sema3d-mediated, but not Sema3e-mediated, cytoskeletal reorganization, and siRNA knockdown of Nrp1 abrogates Sema3d-mediated, but not Sema3e-mediated, inhibition of tubulogenesis. On the other hand, endothelial cells deficient in Plxnd1 are resistant to endothelial repulsion mediated by Sema3e but not Sema3d. Unlike Sema3e, Sema3d incubation results in phosphorylation of Akt in human umbilical vein endothelial cells, and inhibition of the PI3K/Akt pathway blocks the endothelial guidance and cytoskeletal reorganization functions of Sema3d but not Sema3e. © 2014 by The American Society for Biochemistry and Molecular Biology, Inc.
dc.language.isoen
dc.publisherAMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
dc.sourceElements
dc.subjectScience & Technology
dc.subjectLife Sciences & Biomedicine
dc.subjectBiochemistry & Molecular Biology
dc.subjectGROWTH CONE COLLAPSE
dc.subjectVASCULAR DEVELOPMENT
dc.subjectCANCER CELLS
dc.subjectANGIOGENESIS
dc.subjectNEUROPILIN-1
dc.subjectBRAIN
dc.subjectATTRACTION
dc.subjectINHIBITION
dc.subjectEXPRESSION
dc.subjectRECEPTORS
dc.typeArticle
dc.date.updated2021-09-22T02:30:11Z
dc.contributor.departmentENGLISH LANGUAGE & LITERATURE
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.description.doi10.1074/jbc.M113.544833
dc.description.sourcetitleJOURNAL OF BIOLOGICAL CHEMISTRY
dc.description.volume289
dc.description.issue26
dc.description.page17971-17979
dc.published.statePublished
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