Restoration of Podocyte Structure and Improvement of Chronic Renal Disease in Transgenic Mice Overexpressing Renin 英文参考文献.docVIP

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Restoration of Podocyte Structure and Improvement of Chronic Renal Disease in Transgenic Mice Overexpressing Renin 英文参考文献.doc

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Restoration of Podocyte Structure and Improvement of Chronic Renal Disease in Transgenic Mice Overexpressing Renin 英文参考文献

RestorationofPodocyteStructureandImprovementof ChronicRenalDiseaseinTransgenicMice OverexpressingRenin Anne-Ce′cileHuby1,Maria-PiaRastaldi2,KathleenCaron3,OliverSmithies4,Jean-ClaudeDussaule1,5,6, ChristosChatziantoniou1,5 * 1INSERM UMR 702, Paris, France, 2Fondazione IRCCS Ospedale Maggiore Policlinico Fondazione D’Amico per la Ricerca sulle Malattie Renali, Milano, Italy, 3Department of Molecular and Cell Physiology, University of North Carolina, Chapel Hill, North Carolina, United States of America, 4Department of Pathology and LaboratoryMedicine,UniversityofNorthCarolina,ChapelHill,NorthCarolina,UnitedStatesofAmerica,5Universite′PierreetMarieCurie-ParisVI,UMRS702,Paris,France, 6AP-HP,Ho?pitalSt-Antoine,DepartmentofPhysiology,Paris,France Abstract Background:Proteinuriaisamajormarkerofthedeclineofrenalfunctionandanimportantriskfactorofcoronaryheart disease.Elevatedproteinuriaisassociatedtothedisruptionofslit-diaphragmandlossofpodocytefootprocesses,structural alterationsthatareconsideredirreversible.Theobjectiveofthepresentstudywastoinvestigatewhetherproteinuriacanbe reversedandtoidentifythestructuralmodificationsandthegene/proteinregulationassociatedtothisreversal. Methodology/PrincipalFindings: Weusedanoveltransgenicstrainofmouse(RenTg)thatoverexpressesreninataconstant high level.Attheageof12-month, RenTgmiceshowed establishedlesionstypicalofchronicrenaldiseasesuch asperi- vascularandperiglomerularinflammation,glomerularischemia,glomerulosclerosis,mesangialexpansionandtubulardilation. Ultrastructuralanalysisindicatedabnormalheterogeneityofbasementmembranethicknessanddisappearanceofpodocyte foot processes. These structural alterations were accompanied by decreased expressions of proteins specific of podocyte (nephrin,podocin),ortubularepithelialcell(E-cadherinandmegalin)integrity.Inaddition,sinceTGFbisconsideredthemajor pro-fibroticagentinrenaldiseaseandsinceexogenousadministrationofBMP7isreportedtoantagonizetheTGFb-induced phenotypechangesinkidney,weha