Quiescent Fibroblasts Are More Active in Mounting Robust Inflammatory Responses Than Proliferative Fibroblasts 英文参考文献.docVIP

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Quiescent Fibroblasts Are More Active in Mounting Robust Inflammatory Responses Than Proliferative Fibroblasts 英文参考文献.doc

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Quiescent Fibroblasts Are More Active in Mounting Robust Inflammatory Responses Than Proliferative Fibroblasts 英文参考文献

QuiescentFibroblastsAreMoreActiveinMounting RobustInflammatoryResponsesThanProliferative Fibroblasts Bo-RuiChen1,2.,Huei-HsuanCheng1.,Wei-ChungLin1,Kai-HsuanWang1,Jun-YangLiou1 ,Pei- FengChen1,KennethK.Wu1,2* 1InstituteofCellularandSystemMedicine,NationalHealthResearchInstitutes,Zhunan,Miaoli,Taiwan,2InstituteofBiotechnology,NationalTsingHuaUniversity,Hsin- Chu,Taiwan Abstract Quiescent cellsareconsideredtobe dormant. However,recentstudies suggestthatquiescent fibroblastspossess active metabolic profile and certain functional characteristics. We previously observed that serum-starved quiescent fibroblasts respondtoproinflammatorystimulibyrobustexpressionofcyclooxygenase-2(COX-2),whichdeclinesafterthequiescent fibroblastsaredriventoproliferation.Inthisstudy,weelucidatedtheunderlyingsignalingandtranscriptionalmechanism andidentifiedbymicroarraygeneswithsimilardifferentialexpression. Byusingpharmacologicalinhibitorscoupledwith genesilencing,weuncoveredthekeyroleofproteinkinaseCd(PKCd)andextracellularsignalregulatedproteinkinase1/2 (ERK1/2)signalinginmediatingCOX-2expressioninquiescentcells.Surprisingly,COX-2expressioninproliferativecellswas notblocked by PKCdorERK1/2inhibitors duetointrinsicinhibition ofPKCdandERK1/2in proliferative cells. Restrained COX-2transcriptioninproliferativecellswasattributabletoreducedNF-kBbinding.Microarrayanalysisidentified35genes whose expressions were more robust in quiescent than in proliferative cells. A majority of those genes belong to proinflammatorycytokines,chemokines,adhesivemoleculesandmetalloproteinases,whichrequireNF-kBfortranscription. Quiescent fibroblasts had a higher migratory activity than proliferative fibroblasts as determined by the transwell assay. Selective COX-2 inhibition reduced migration which was restored by prostaglandin E2. As COX-2 and inflammatory mediators induce DNA oxidation, we measured 8-hydroxydeoxyguanosine (8-OHdG) in quiescent vs. proliferative fibroblasts.PMA-induced8-OHdGaccumulationw