Proteinuria Triggers Renal Lymphangiogenesis Prior to the Development of Interstitial Fibrosis 英文参考文献.docVIP

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Proteinuria Triggers Renal Lymphangiogenesis Prior to the Development of Interstitial Fibrosis 英文参考文献.doc

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Proteinuria Triggers Renal Lymphangiogenesis Prior to the Development of Interstitial Fibrosis 英文参考文献

ProteinuriaTriggersRenalLymphangiogenesisPriorto theDevelopmentofInterstitialFibrosis SalehYazdani1*,FaribaPoosti2,AndreaB.Kramer1,KatarinaMirkovic′1,ArjanJ.Kwakernaak1, MennoHovingh1,MaartjeC.J.Slagman1,KlaasA.Sjollema3,MartinH.deBorst1,GerjanNavis1, HarryvanGoor2,JacobvandenBorn1 1DivisionofNephrology,DepartmentofMedicine,UniversityMedicalCenterGroningen,UniversityofGroningen,Groningen,TheNetherlands,2DivisionofPathology, DepartmentofPathologyandMedicalBiology,UniversityMedicalCenterGroningen,UniversityofGroningen,Groningen,TheNetherlands,3MicroscopyandImaging Center,UniversityMedicalCenterGroningen,UniversityofGroningen,Groningen,TheNetherlands Abstract Proteinuria is an important cause of progressive tubulo-interstitial damage. Whether proteinuria could trigger a renal lymphangiogenic response has not been established. Moreover, the temporal relationship between development of fibrosis,inflammationandlymphangiogenesisinchronicprogressivekidneydiseaseisnotclearyet.Therefore,weevaluated thetimecourseoflymphvessel(LV)formationinrelationtoproteinuriaandinterstitialdamageinaratmodelofchronic unilateraladriamycinnephrosis.Proteinuriaandkidneyswereevaluatedupto30weeksafterinductionofnephrosis.LVs wereidentifiedbypodoplanin/VEGFR3doublestaining.After6weeksproteinuriawaswell-established,withoutinfluxof interstitial macrophages and myofibroblasts, collagen deposition, osteopontin expression (tubular activation) or LV formation.At12weeks,a,3-foldincreaseincorticalLVdensitywasfound(p,0.001),graduallyincreasingovertime.This correspondedwithasignificantincreaseintubularosteopontinexpression(p,0.01)andinterstitialmyofibroblastnumbers (p,0.05),whereascollagendepositionandmacrophagenumberswerenotyetincreased.VEGF-Cwasmostlyexpressedby tubularcellsratherthaninterstitialcells.CulturedtubularcellsstimulatedwithFCSshowedadose-dependentincreasein mRNAandproteinexpressionofVEGF-Cwhichwasnotobservedbyhumanalbuminstimulation.Weconcludethatchronic proteinuria provoked lymphangiogenesis