A Ribosomal S-6 Kinase–Mediated Signal to CEBP-β Is Critical for the Development of Liver Fibrosis 英文参考文献.docVIP
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A Ribosomal S-6 Kinase–Mediated Signal to CEBP-β Is Critical for the Development of Liver Fibrosis 英文参考文献
ARibosomalS-6Kinase–MediatedSignaltoC/EBP-bIs
CriticalfortheDevelopmentofLiverFibrosis
MartinaBuck1,2*,MarioChojkier1,2
1Department of Medicine and Moores Cancer Center, University of California at San Diego, La Jolla, California, United States of America,
2DepartmentofMedicine,VeteransAffairs(VA)HealthcareCenter,SanDiego,California,UnitedStatesofAmerica
Background.Inresponsetoliverinjury,hepaticstellatecell(HSC)activationcausesexcessiveliverfibrosis.Hereweshowthat
activation of RSK and phosphorylation of C/EBPb on Thr217 in activated HSC is critical for the progression of liver fibrosis.
Methodology/Principal Findings. Chronic treatment with the hepatotoxin CCl4 induced severe liver fibrosis in C/EBPb+/+
micebutnotinmiceexpressingC/EBPb-Ala217,anon-phosphorylatableRSK-inhibitorytransgene.C/EBPb-Ala217waspresent
within the death receptor complex II, with active caspase 8, and induced apoptosis of activated HSC. The C/EBPb-Ala217
peptidesdirectlystimulatedcaspase8activationinacell-freesystem.C/EBPb+/+micewithCCl4-inducedsevereliverfibrosis,
whilecontinuingonCCl4,weretreatedwithacellpermeantRSK-inhibitorypeptidefor4or8weeks.ThepeptideinhibitedRSK
activation,stimulatingapoptosisofHSC,preventingprogressionandinducingregressionofliverfibrosis.Wefoundasimilar
activationofRSKandphosphorylationofhumanC/EBPbonThr266(humanphosphoacceptor)inactivatedHSCinpatientswith
severe liver fibrosis but not in normal livers, suggesting that this pathway may also be relevant in human liver fibrosis.
Conclusions/Significance.ThesedataindicatethattheRSK-C/EBPbphosphorylationpathwayiscriticalforthedevelopment
ofliverfibrosisandsuggestapotentialtherapeutictarget.
Citation: Buck M, Chojkier M (2007) A Ribosomal S-6 Kinase–Mediated Signal to C/EBP-b Is Critical for the Development of Liver Fibrosis. PLoS
ONE2(12):e1372.doi:10.1371/journal.pone.0001372
INTRODUCTION
ingprogressionandinducingregressionofliverfibrosiscompared
tocontrolmicetreatedwithCCl4.Wefoundsimilaractivationof
RSK and phospho
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