Rosiglitazone Inhibits Transforming Growth Factor-β1 Mediated Fibrogenesis in ADPKD Cyst-Lining Epithelial Cells 英文参考文献.docVIP
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Rosiglitazone Inhibits Transforming Growth Factor-β1 Mediated Fibrogenesis in ADPKD Cyst-Lining Epithelial Cells 英文参考文献
RosiglitazoneInhibitsTransformingGrowthFactor-b1
MediatedFibrogenesisinADPKDCyst-LiningEpithelial
Cells
YaweiLiu.,BingDai.,ChenggangXu.,LiliFu,ZhenhaoHua,ChanglinMei*
DivisionofNephrology,NephrologyInstituteofPLA,ShanghaiChangzhengHospital,SecondMilitaryMedicalUniversity,Shanghai,China
Abstract
Background:Interstitialfibrosisplaysanimportantroleinprogressiverenaldysfunctioninautosomaldominantpolycystic
kidney disease (ADPKD). In our previous studies, we confirmed that PPAR-c agonist, rosiglitazone could protect renal
functionand prolong thesurvival of aslowly progressive ADPKD animalmodel by reducing renal fibrosis. However, the
mechanismremainsunknown.
Methods: Primary culture epithelial cells pretreated with TGF-b1 were incubated with rosiglitazone. Extracellular matrix
proteinsweredetectedusingreal-timePCRandWesternblotting.MAPKandSmad2phosphorylationweremeasuredwith
western blot. ERK1/2 pathway and P38 pathway were inhibited with the specific inhibitors PD98059 and SB203580. The
Smad2pathwaywasblockedwiththesiRNA.ToaddresswhetherPPAR-cagonist-mediatedinhibitionofTGF-b1–induced
collagentypeIexpressionwasmediatedthroughaPPAR-cdependentmechanism,geneticandpharmaceuticalapproaches
wereusedtoblocktheactivityofendogenousPPARc.
Results: TGF-b1-stimulated collagen type I and fibronectin expression of ADPKD cyst-lining epithelia were inhibited by
rosiglitazone in a dosage-dependent manner. Smad2, ERK1/2 and P38 pathways were activated in response to TGF-b1;
however,TGF-b1hadlittleeffectonJNKpathway.RosiglitazonesuppressedTGF-b1inducedSmad2activation,whileERK1/2
and P38MAPK signals remained unaffected. Rosiglitazone could also attenuate TGF-b1-stimulated collagen type I and
fibronectinexpressioninprimaryrenaltubularepithelialcells,buthadnoeffectonTGF-b1–inducedactivationofSmad2,
ERK1/2andP38pathways.TherewasnocrosstalkbetweentheSmad2andMAPKpathwaysinADPKDcyst-liningepithelial
cells.TheseinhibitoryeffectsofrosiglitazonewerereversedbythePPARcspecificantagonistGW9662andPPA
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