Prostaglandin E2 Promotes Endothelial Differentiation from Bone Marrow-Derived Cells through AMPK Activation 英文参考文献.docVIP

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Prostaglandin E2 Promotes Endothelial Differentiation from Bone Marrow-Derived Cells through AMPK Activation 英文参考文献.doc

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Prostaglandin E2 Promotes Endothelial Differentiation from Bone Marrow-Derived Cells through AMPK Activation 英文参考文献

ProstaglandinE2PromotesEndothelialDifferentiation fromBoneMarrow-DerivedCellsthroughAMPK Activation ZhenjiuZhu1.,ChenglaiFu1.,XiaoxiaLi1,YimengSong1,ChenghongLi1,MinghuiZou2,YoufeiGuan1*, YiZhu1* 1KeyLaboratoryofMolecularCardiovascularSciencesofEducationMinistry,DepartmentofPhysiologyandPathophysiology,PekingUniversityHealthScienceCenter, Beijing,China, 2Division of Endocrinology and Diabetes, Departmentof Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United StatesofAmerica Abstract Prostaglandin E2 (PGE2) has been reported to modulate angiogenesis, the process of new blood vessel formation, by promoting proliferation, migration and tube formation of endothelial cells. Endothelial progenitor cells are known as a subsetofcirculatingbonemarrowmononuclearcellsthathavethecapacitytodifferentiateintoendothelialcells.However, themechanismunderlyingthestimulatoryeffectsofPGE2anditsspecificreceptorsonbonemarrow-derivedcells(BMCs)in angiogenesishasnotbeenfullycharacterized.TreatmentwithPGE2significantlyincreasedthedifferentiationandmigration ofBMCs.Also,themarkersofdifferentiationtoendothelialcells,CD31andvonWillebrandfactor,andthegenesassociated with migration, matrix metalloproteinases 2 and 9, were significantly upregulated. This upregulation was abolished by dominant-negative AMP-activated protein kinase (AMPK) and AMPK inhibitor but not protein kinase, a inhibitor. As a functionalconsequenceofdifferentiationandmigration,thetubeformationofBMCswasreinforced.Alongwithaltered BMCs functions, phosphorylation and activation of AMPK and endothelial nitric oxide synthase, the target of activated AMPK,werebothincreasedwhichcouldbeblockedbyEP4blockingpeptideandsimulatedbytheagonistofEP4butnot EP1,EP2orEP3.Thepro-angiogenicroleofPGE2couldberepressedbyEP4blockingpeptideandretardedinEP4+/2 mice. Therefore,bypromotingthedifferentiationandmigrationofBMCs,PGE2reinforcedtheirneovascularizationbybindingto thereceptorofEP4inanAMPK-dependentmanner.PGE2may