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