REX-1 Expression and p38 MAPK Activation Status Can Determine ProliferationDifferentiation Fates in Human Mesenchymal Stem Cells 英文参考文献.docVIP

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REX-1 Expression and p38 MAPK Activation Status Can Determine ProliferationDifferentiation Fates in Human Mesenchymal Stem Cells 英文参考文献.doc

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REX-1 Expression and p38 MAPK Activation Status Can Determine ProliferationDifferentiation Fates in Human Mesenchymal Stem Cells 英文参考文献

REX-1Expressionandp38MAPKActivationStatusCan DetermineProliferation/DifferentiationFatesinHuman MesenchymalStemCells DilliRamBhandari1,2.,Kwang-WonSeo1,2.,Kyoung-HwanRoh1,2.,Ji-WonJung1,2,Soo-KyungKang3, Kyung-SunKang1,2 * 1AdultStemCellResearch,CollegeofVeterinaryMedicine,SeoulNationalUniversity,Seoul,RepublicofKorea,2LaboratoryofStemCellandTumorBiology,Department of Veterinary Public Health, College of Veterinary Medicine, Seoul National University, Seoul, Korea, 3Laboratory of Veterinary Biotechnology, College of Veterinary MedicineandBK21ProgramforVeterinaryScience,SeoulNationalUniversity,Seoul,Korea Abstract Background:REX1/ZFP42isawell-knownembryonicstemcell(ESC)marker.However,theroleofREX1,itself,isrelatively unknownbecausethefunctionofREX1hasonlybeenreportedinthedifferentiationofESCsviaSTATsignalingpathways. Humanmesenchymalstemcells(hMSCs)isolatedfromyoungtissuesandcancercellsexpressREX1. Methodology/PrincipalFinding:Humanumbilicalcordblood-derivedMSCs(hUCB-MSCs)andadiposetissue-derivedMSCs (hAD-MSCs)stronglyexpressREX1andhavealoweractivationstatusofp38MAPK,butbonemarrow-derivedMSCs(hBM- MSCs) have weak REX1 expression and higher activation of p38 MAPK. These results indicated that REX1 expression in hMSCswaspositivelycorrelatedwithproliferationratesbutinverselycorrelatedwiththephosphorylationofp38MAPK.In hUCB-MSCs,therolesofREX1andp38MAPKwereinvestigated,andaknockdownstudywasperformedusingalentiviral vector-based small hairpin RNA (shRNA). After REX1 knockdown, decreased cell proliferation was observed. In REX1 knocked-down hUCB-MSCs, the osteogenic differentiation ability deteriorated, but the adipogenic potential increased or wassimilartothatobservedinthecontrols.Thephosphorylationofp38MAPKinhUCB-MSCssignificantlyincreasedafter REX1 knockdown. After p38 MAPK inhibitor treatment, the cell growth in REX1 knocked-down hUCB-MSCs almost recovered, and the suppressed expression levels of CDK2 and CCND1 were also restored. The expression of MKK3, an upstreamr