Hepatocyte Growth Factor Increases Osteopontin Expression in Human Osteoblasts through PI3K, Akt, c-Src, and AP-1 Signaling Pathway 英文参考文献.docVIP

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Hepatocyte Growth Factor Increases Osteopontin Expression in Human Osteoblasts through PI3K, Akt, c-Src, and AP-1 Signaling Pathway 英文参考文献.doc

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Hepatocyte Growth Factor Increases Osteopontin Expression in Human Osteoblasts through PI3K, Akt, c-Src, and AP-1 Signaling Pathway 英文参考文献

HepatocyteGrowthFactorIncreasesOsteopontin ExpressioninHumanOsteoblaststhroughPI3K,Akt,c- Src,andAP-1SignalingPathway Hsien-TeChen1,2,3,Hsi-KaiTsou3,4,5,Chia-HaoChang6,Chih-HsinTang7,8* 1SchoolofChineseMedicine,CollegeofChineseMedicine,ChinaMedicalUniversity,Taichung,Taiwan,2DepartmentofOrthopedicSurgery,ChinaMedicalUniversity Hospital, Taichung, Taiwan, 3Department of Materials Science and Engineering, Feng Chia University, Taichung, Taiwan, 4Department of Neurosurgery, Taichung Veterans General Hospital, Taichung, Taiwan, 5Center for General Education, Jen-Teh Junior College of Medicine, Nursing and Management, Miaoli County, Taiwan, 6DepartmentofOrthopedicSurgery,Chang-HwaHospital,DepartmentofHealthExecutiveYuan,Chang-HwaCounty,Taiwan,7DepartmentofPharmacology,Schoolof Medicine,ChinaMedicalUniversity,Taichung,Taiwan,8GraduateInstituteofBasicMedicalScience,ChinaMedicalUniversity,Taichung,Taiwan Abstract Background:Hepatocytegrowthfactor(HGF)hasbeendemonstratedtostimulateosteoblastproliferationandparticipated boneremodeling.Osteopontin(OPN)isasecretedphosphoglycoproteinthatbelongstotheSIBLINGfamilyandispresent duringbonemineralization.However,theeffectsofHGFonOPNexpressioninhumanosteoblastsarelargeunknown. Methodology/Principal Findings: Here we found that HGF induced OPN expression in human osteoblasts dose- dependently. HGF-mediated OPN production was attenuated by c-Met inhibitor and siRNA. Pretreatment of osteoblasts with PI3K inhibitor (Ly294002), Akt inhibitor, c-Src inhibitor (PP2), or AP-1 inhibitor (curcumin) blocked the potentiating actionofHGF.StimulationofosteoblastswithHGFenhancedPI3K,Akt,andc-Srcactivation.Inaddition,incubationofcells withHGFalsoincreasedc-Junphosphorylation,AP-1-luciferaseactivity,andc-JunbindingtotheAP-1elementontheOPN promoter.HGF-mediatedAP-1-luciferaseactivityandc-JunbindingtotheAP-1elementwasreducedbyc-Metinhibitor, Ly294002,Aktinhibitor,andPP2. Conclusions/Significance: Our results suggest that theinteraction between HGF and