2014
Podocyte-Specific VEGF-A Gain of Function Induces Nodular Glomerulosclerosis in eNOS Null Mice
Veron D, Aggarwal PK, Velazquez H, Kashgarian M, Moeckel G, Tufro A. Podocyte-Specific VEGF-A Gain of Function Induces Nodular Glomerulosclerosis in eNOS Null Mice. Journal Of The American Society Of Nephrology 2014, 25: 1814-1824. PMID: 24578128, PMCID: PMC4116059, DOI: 10.1681/asn.2013070752.Peer-Reviewed Original ResearchConceptsNodular glomerulosclerosisGain of functionEndothelial nitric oxide synthase knockout miceNitric oxide synthase knockout miceGlomerular basement membrane thickeningENOS-null miceSynthase knockout miceBasement membrane thickeningWild-type miceCollagen IVArteriolar hyalinosisGlomerular nodulesGlomerular VEGFKimmelstiel-WilsonPronounced albuminuriaCreatinine clearanceRenal failureDiabetic nephropathyENOS deficiencyMassive proteinuriaDiabetic milieuMembrane thickeningPodocyte effacementDeposition of lamininKnockout mice
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
2010
Overexpression 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
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