2010
Induction of Podocyte VEGF164 Overexpression at Different Stages of Development Causes Congenital Nephrosis or Steroid-Resistant Nephrotic Syndrome
Veron D, Reidy K, Marlier A, Bertuccio C, Villegas G, Jimenez J, Kashgarian M, Tufro A. Induction of Podocyte VEGF164 Overexpression at Different Stages of Development Causes Congenital Nephrosis or Steroid-Resistant Nephrotic Syndrome. American Journal Of Pathology 2010, 177: 2225-2233. PMID: 20829436, PMCID: PMC2966782, DOI: 10.2353/ajpath.2010.091146.Peer-Reviewed Original ResearchConceptsNephrotic syndromePodocyte effacementTransgenic miceSteroid-resistant nephrotic syndromeEndothelial cellsSingle transgenic miceMultiple renal diseasesSwollen endothelial cellsCongenital nephrotic syndromeVascular endothelial growthInducible transgenic miceNormal endothelial cellsGlomerular filtration barrierRenal diseasePathogenic rolePodocyte lossMice expressMassive albuminuriaEndothelial growthCongenital nephrosisMinimal changesFoot processesMiceGlomerulomegalyAlbuminuriaOverexpression of VEGF-A in podocytes of adult mice causes glomerular disease
Veron D, Reidy KJ, Bertuccio C, Teichman J, Villegas G, Jimenez J, Shen W, Kopp JB, Thomas DB, Tufro A. Overexpression of VEGF-A in podocytes of adult mice causes glomerular disease. Kidney International 2010, 77: 989-999. PMID: 20375978, DOI: 10.1038/ki.2010.64.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAnimalsAutocrine CommunicationDiabetic NephropathiesGenotypeGlomerular Basement MembraneKidney DiseasesMatrix Metalloproteinase 9Membrane ProteinsMiceMice, TransgenicParacrine CommunicationPhenotypePhosphorylationPodocytesProtein BindingProteinuriaSignal TransductionUp-RegulationVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2ConceptsGlomerular diseaseAdult miceGlomerular basement membrane thickeningMurine diabetic nephropathyBasement membrane thickeningGlomerular endothelial cellsAdult transgenic miceOverexpression of VEGFExcessive VEGFDiabetic nephropathyGlomerular filtration barrierMesangial expansionPathogenic roleMetalloproteinase-9Functional abnormalitiesMembrane thickeningPodocyte effacementNephrin expressionReceptor 2Transgenic miceWhole kidneyGlomerular phenotypeEndothelial cellsParacrine VEGFVEGF
2009
Semaphorin3a regulates endothelial cell number and podocyte differentiation during glomerular development
Reidy KJ, Villegas G, Teichman J, Veron D, Shen W, Jimenez J, Thomas D, Tufro A. Semaphorin3a regulates endothelial cell number and podocyte differentiation during glomerular development. Development 2009, 136: 3979-3989. PMID: 19906865, PMCID: PMC2778745, DOI: 10.1242/dev.037267.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCell CountCell DifferentiationCell NucleusCoculture TechniquesEndothelial CellsFluorescent Antibody Technique, DirectFluorescent DyesGene DeletionGene Expression Regulation, DevelopmentalGriffoniaImmunohistochemistryIn Situ Nick-End LabelingIndolesKidney GlomerulusMiceMice, KnockoutMice, Mutant StrainsMice, TransgenicPlant LectinsPodocytesRatsRecombinant ProteinsSemaphorin-3AConceptsVascular patterningPodocyte differentiationNegative regulatorNormal glomerular filtration barrierGlomerular developmentEssential negative regulatorEndothelial cell survivalFunction mouse modelsTight regulationEndothelial cell apoptosisUreteric budMature podocytesVascular developmentCell survivalCrucial roleGuidance proteinsSlit diaphragmCell apoptosisGlomerular filtration barrierRegulatorFiltration barrierGlomerular endothelial cell apoptosisCell numberEndothelial cellsEndothelial cell number
2007
Semaphorin3a disrupts podocyte foot processes causing acute proteinuria
Tapia R, Guan F, Gershin I, Teichman J, Villegas G, Tufro A. Semaphorin3a disrupts podocyte foot processes causing acute proteinuria. Kidney International 2007, 73: 733-740. PMID: 18075495, DOI: 10.1038/sj.ki.5002726.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsCytoskeletal ProteinsDown-RegulationGlomerular Basement MembraneGlomerular Filtration RateIntracellular Signaling Peptides and ProteinsMaleMembrane ProteinsMiceMice, Inbred StrainsPermeabilityPodocytesProteinuriaRecombinant ProteinsSemaphorin-3AVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Receptor-2ConceptsPodocyte foot process effacementNephrotic range proteinuriaEndothelial cell damageVascular endothelial growth factorSlit diaphragm protein podocinFoot process effacementEndothelial growth factorReceptor 2 signalingVascular endothelial growth factor receptor 2 signalingAcute proteinuriaRange proteinuriaReceptor expressionVascular endothelial growth factor 165Process effacementBarrier homeostasisAdult mouse kidneyUltrastructural abnormalitiesSemaphorin3AEndothelial cellsCell damageGrowth factorMouse kidneyGuidance proteinsProteinuriaDownregulation
2006
Semaphorin 3C regulates endothelial cell function by increasing integrin activity
Banu N, Teichman J, Dunlap‐Brown M, Villegas G, Tufro A, Banu N, Teichman J, Dunlap‐Brown M, Villegas G, Tufro A. Semaphorin 3C regulates endothelial cell function by increasing integrin activity. The FASEB Journal 2006, 20: 2150-2152. PMID: 16940438, DOI: 10.1096/fj.05-5698fje.Peer-Reviewed Original ResearchConceptsSema 3CEndothelial cell functionDirectional migrationStarvation-induced apoptosisCell functionCapillary-like network formationCardiovascular patterningClass 3 semaphorinsIntegrin phosphorylationSerine phosphorylationCollagen I gelsVascular morphogenesisEndothelial cellsMouse glomerular endothelial cellsIntegrin activityGuidance proteinsEndothelial cell proliferationIntegrin inhibitionCaspase-3Cell proliferationSitu markerTube formationSemaphorin 3CPhosphorylationGrowth factor