Activation of the Connective Tissue Growth Factor (CTGF)-Transforming Growth Factor β 1 (TGF-β 1) Axis in Hepatitis C Virus-Expressing Hepatocytes 英文参考文献.docVIP

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Activation of the Connective Tissue Growth Factor (CTGF)-Transforming Growth Factor β 1 (TGF-β 1) Axis in Hepatitis C Virus-Expressing Hepatocytes 英文参考文献.doc

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Activation of the Connective Tissue Growth Factor (CTGF)-Transforming Growth Factor β 1 (TGF-β 1) Axis in Hepatitis C Virus-Expressing Hepatocytes 英文参考文献

ActivationoftheConnectiveTissueGrowthFactor (CTGF)-TransformingGrowthFactorb1(TGF-b1)Axisin HepatitisCVirus-ExpressingHepatocytes TirumuruNagaraja1.,LiChen2.,AnuradhaBalasubramanian3,JeromeE.Groopman3,KalpanaGhoshal4, SamsonT.Jacob4,AndrewLeask5,DavidR.Brigstock2*,AppakkudalR.Anand1*,RameshK.Ganju1* 1DepartmentofPathology,OhioStateUniversityWexnerMedicalCenter,Columbus,Ohio,UnitedStatesofAmerica,2CenterforClinicalandTranslationalResearch,The Research Institute at Nationwide Children’s Hospital, Columbus, Ohio, United States of America, 3Division of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States of America, 4Department of Molecular and Cellular Biochemistry, The Ohio State University, Columbus,Ohio,UnitedStatesofAmerica,5SchulichSchoolofMedicineandDentistry,UniversityofWesternOntario,London,Ontario,Canada Abstract Background: The pro-fibrogenic cytokine connective tissue growth factor (CTGF) plays an important role in the developmentandprogressionoffibrosisinmanyorgansystems,includingliver.However,itsroleinthepathogenesisof hepatitisCvirus(HCV)-inducedliverfibrosisremainsunclear. Methods:Inthepresentstudy,weassessedCTGFexpressioninHCV-infectedhepatocytesusingrepliconcellscontaining full-lengthHCVgenotype1andtheinfectiousHCVcloneJFH1(HCVgenotype2)byreal-timePCR,Westernblotanalysisand confocalmicroscopy.Weevaluatedtransforminggrowthfactorb1(TGF-b1)asakeyupstreammediatorofCTGFproduction usingneutralizingantibodiesandshRNAs.WealsodeterminedthesignalingmoleculesinvolvedinCTGFproductionusing variousimmunologicaltechniques. Results: We demonstrated an enhanced expression of CTGF in two independent models of HCV infection. We also demonstrated that HCV induced CTGF expression in a TGF-b1-dependent manner. Further dissection of the molecular mechanisms revealed that CTGF production was mediated through sequential activation of MAPkinase and Smad- dependentpathways.Finally,todeterminewhetherCTGFregul