2016
The Robo4 cytoplasmic domain is dispensable for vascular permeability and neovascularization
Zhang F, Prahst C, Mathivet T, Pibouin-Fragner L, Zhang J, Genet G, Tong R, Dubrac A, Eichmann A. The Robo4 cytoplasmic domain is dispensable for vascular permeability and neovascularization. Nature Communications 2016, 7: 13517. PMID: 27882935, PMCID: PMC5123080, DOI: 10.1038/ncomms13517.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCapillary PermeabilityDiabetic RetinopathyIntercellular Signaling Peptides and ProteinsMiceMice, KnockoutNeovascularization, PathologicNerve Tissue ProteinsNetrin ReceptorsOxygen Inhalation TherapyPhosphorylationReceptors, Cell SurfaceReceptors, ImmunologicRetinal DiseasesRetinopathy of PrematuritySignal TransductionVascular Endothelial Growth Factor Receptor-2Wound HealingConceptsCytoplasmic domainOxygen-induced retinopathyVascular permeabilityRetinopathy of prematurityTransmembrane receptorsWound healingDiabetic wound healingCutaneous wound healingDiabetic patientsUNC5B receptorRobo4Transgenic miceTissue revascularizationRevascularizationVessel permeabilityRetinopathyMiceHealingNeovascularizationReceptorsDomainPhosphorylationDeletionPrematurityPathwaymiR-182 Modulates Myocardial Hypertrophic Response Induced by Angiogenesis in Heart
Li N, Hwangbo C, Jaba IM, Zhang J, Papangeli I, Han J, Mikush N, Larrivée B, Eichmann A, Chun HJ, Young LH, Tirziu D. miR-182 Modulates Myocardial Hypertrophic Response Induced by Angiogenesis in Heart. Scientific Reports 2016, 6: 21228. PMID: 26888314, PMCID: PMC4758045, DOI: 10.1038/srep21228.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCardiomegalyEndotheliumMechanistic Target of Rapamycin Complex 1Membrane ProteinsMiceMice, KnockoutMicroRNAsMultiprotein ComplexesMyocytes, CardiacNeovascularization, PathologicNitric OxideNitric Oxide Synthase Type IIIProteinsProto-Oncogene Proteins c-aktRGS ProteinsTOR Serine-Threonine KinasesUp-RegulationConceptsHypertrophic responseMiR-182Myocardial hypertrophyEndothelial-cardiomyocyte crosstalkLV pressure overloadEndothelium-derived NOPlacental growth factorMyocardial hypertrophic responseDevelopment of hypertrophyDegradation of regulatorsMiR-182 targetsHemodynamic demandsPressure overloadPlGF expressionBlood supplyParacrine actionCardiomyocyte hypertrophyMyocardial angiogenesisCardiac angiogenesisTreatment inhibitsHypertrophyAKT/mTORC1 pathwaysNovel targetAkt/Growth factor
2013
The Neuropilin 1 Cytoplasmic Domain Is Required for VEGF-A-Dependent Arteriogenesis
Lanahan A, Zhang X, Fantin A, Zhuang Z, Rivera-Molina F, Speichinger K, Prahst C, Zhang J, Wang Y, Davis G, Toomre D, Ruhrberg C, Simons M. The Neuropilin 1 Cytoplasmic Domain Is Required for VEGF-A-Dependent Arteriogenesis. Developmental Cell 2013, 25: 156-168. PMID: 23639442, PMCID: PMC3774154, DOI: 10.1016/j.devcel.2013.03.019.Peer-Reviewed Original ResearchAnimalsArteriesCells, CulturedCytoplasmEndocytosisEndosomesEndothelium, VascularMAP Kinase Signaling SystemMiceMorphogenesisNeovascularization, PathologicNeuropilin-1PhosphorylationSignal TransductionTransferrinVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2Vesicular Transport Proteins