Secretogranin II; a Protein Increased in the Myocardium and Circulation in Heart Failure with Cardioprotective Properties 英文参考文献.docVIP

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Secretogranin II; a Protein Increased in the Myocardium and Circulation in Heart Failure with Cardioprotective Properties 英文参考文献.doc

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Secretogranin II; a Protein Increased in the Myocardium and Circulation in Heart Failure with Cardioprotective Properties 英文参考文献

SecretograninII;aProteinIncreasedintheMyocardium andCirculationinHeartFailurewithCardioprotective Properties HelgeR?sj?1,2*,MatsStridsberg3,GeirFlorholmen2,4,Ka?re-OlavStensl?kken5 ,Anett Helleb?Ottesen1,2,4,IvarSjaastad2,4,CathrineHusberg2,4,MaiBrittDahl1,2,6,Erik?ie2,7 WilliamE.Louch2,4,Torbj?rnOmland1,2,GeirChristensen2,4 , 1DivisionofMedicine,AkershusUniversityHospital,L?renskog,Norway,2CenterforHeartFailureResearchandK.G.JebsenCardiacResearchCentre,InstituteofClinical Medicine,UniversityofOslo,Oslo,Norway,3DepartmentofMedicalSciences,UppsalaUniversity,Uppsala,Sweden,4InstituteforExperimentalMedicalResearch,Oslo UniversityHospital,Ulleva?l,Oslo,Norway,5DepartmentofMolecularBiosciences,UniversityofOslo,Oslo,Norway,6DepartmentofClinicalMolecularBiology,Akershus UniversityHospital,L?renskog,Norway,7ResearchInstituteforInternalMedicine,OsloUniversityHospital,Rikshospitalet,Oslo,Norway Abstract Background:SeveralbeneficialeffectshavebeendemonstratedforsecretograninII(SgII)innon-cardiactissue.Ascardiac productionofchromograninAandB,tworelatedproteins,isincreasedinheartfailure(HF),wehypothesizedthatSgIIcould playaroleincardiovascularpathophysiology. Methodology/PrincipalFindings:SgIIproductionwascharacterizedinapost-myocardialinfarctionheartfailure(HF)mouse model,functionalpropertiesexploredinexperimentalmodels,andcirculatinglevelsmeasuredinmiceandpatientswith stable HF of moderate severity. SgII mRNA levels were 10.5 fold upregulated in the left ventricle (LV) of animals with myocardialinfarctionandHF(p,0.001vs.sham-operatedanimals).SgIIproteinlevelswerealsoincreasedintheLV,butnot inotherorgansinvestigated.SgIIwasproducedinseveralcelltypesinthemyocardiumandcardiomyocytesynthesisofSgII waspotentlyinducedbytransforminggrowthfactor-bandnorepinephrinestimulationinvitro.ProcessingofSgIItoshorter peptideswasenhancedinthefailingmyocardiumduetoincreasedlevelsoftheproteasesPC1/3andPC2andcirculating SgIIlevelswereincreasedinmicewithHF.ExaminingapathophysiologicalroleofSgIIint