2015
Essential Role of X-Box Binding Protein-1 during Endoplasmic Reticulum Stress in Podocytes
Hassan H, Tian X, Inoue K, Chai N, Liu C, Soda K, Moeckel G, Tufro A, Lee AH, Somlo S, Fedeles S, Ishibe S. Essential Role of X-Box Binding Protein-1 during Endoplasmic Reticulum Stress in Podocytes. Journal Of The American Society Of Nephrology 2015, 27: 1055-1065. PMID: 26303067, PMCID: PMC4814187, DOI: 10.1681/asn.2015020191.Peer-Reviewed Original ResearchConceptsX-box binding protein 1Endoplasmic reticulum stress responseEndoplasmic reticulum stressGlomerular filtration barrierPodocyte injuryReticulum stress responseBinding protein 1Reticulum stressProtein 1Filtration barrierFoot process effacementProgressive albuminuriaMouse modelProcess effacementUnfolded protein response pathwayEpithelial cellsNormal glomerular filtration barrierProtein response pathwayEndoplasmic reticulumPodocytesGenetic inactivationXBP1 pathwayInjuryJNK pathwayStress response
2014
Semaphorin3a Promotes Advanced Diabetic Nephropathy
Aggarwal PK, Veron D, Thomas DB, Siegel D, Moeckel G, Kashgarian M, Tufro A. Semaphorin3a Promotes Advanced Diabetic Nephropathy. Diabetes 2014, 64: 1743-1759. PMID: 25475434, PMCID: PMC4407856, DOI: 10.2337/db14-0719.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsChromonesCollagen Type IVDiabetes Mellitus, ExperimentalDiabetic NephropathiesEnzyme-Linked Immunosorbent AssayGene Expression RegulationGene Knockdown TechniquesHumansIntegrin alphaVbeta3LamininMembrane ProteinsMiceMice, KnockoutMicrofilament ProteinsMicrotubule-Associated ProteinsMixed Function OxygenasesNerve Tissue ProteinsPodocytesProteinuriaReceptors, Cell SurfaceRenal InsufficiencySemaphorin-3AWT1 ProteinsXanthonesConceptsAdvanced diabetic nephropathyDiabetic nephropathyRenal insufficiencyDiffuse podocyte foot process effacementPodocyte foot process effacementSevere diabetic nephropathyCollagen IV accumulationPotential therapeutic targetFoot process effacementGlomerular nodulesKimmelstiel-WilsonRenal biopsyGlomerular filtration barrierNodular glomerulosclerosisDiabetic miceMassive proteinuriaNovel therapiesDisease outcomePathogenic factorsTargetable pathwaysTherapeutic targetProcess effacementBarrier abnormalitiesFunction miceNephropathy
2013
Excess Podocyte Semaphorin-3A Leads to Glomerular Disease Involving PlexinA1–Nephrin Interaction
Reidy KJ, Aggarwal PK, Jimenez JJ, Thomas DB, Veron D, Tufro A. Excess Podocyte Semaphorin-3A Leads to Glomerular Disease Involving PlexinA1–Nephrin Interaction. American Journal Of Pathology 2013, 183: 1156-1168. PMID: 23954273, PMCID: PMC3791681, DOI: 10.1016/j.ajpath.2013.06.022.Peer-Reviewed Original Research
2012
Acute Podocyte Vascular Endothelial Growth Factor (VEGF-A) Knockdown Disrupts alphaVbeta3 Integrin Signaling in the Glomerulus
Veron D, Villegas G, Aggarwal PK, Bertuccio C, Jimenez J, Velazquez H, Reidy K, Abrahamson DR, Moeckel G, Kashgarian M, Tufro A. Acute Podocyte Vascular Endothelial Growth Factor (VEGF-A) Knockdown Disrupts alphaVbeta3 Integrin Signaling in the Glomerulus. PLOS ONE 2012, 7: e40589. PMID: 22808199, PMCID: PMC3396653, DOI: 10.1371/journal.pone.0040589.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlood PressureCells, CulturedDown-RegulationDoxycyclineEndotheliumFibronectinsGene Knockdown TechniquesIntegrin alphaVbeta3MiceModels, AnimalNeuropilin-1PhenotypePodocytesProtein BindingProteinuriaRenal InsufficiencyRNA, Small InterferingSignal TransductionVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2ConceptsAcute renal failureVEGF receptor 2Renal failureEndothelial cell swellingPodocyte VEGFUrine VEGFGlomerular filtration barrierLocal injuryPodocyte effacementGlomerular ultrastructureAdult miceDoxycycline exposureReceptor 2Knockdown micePodocyte cell lineControl valuesGlomeruliNeuropilin-1MiceVEGFProtein levelsCell swellingVEGF knockdownProteinuriaFiltration barrier
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