Dilated Cardiomyopathy with Increased SR Ca2+ Loading Preceded by a Hypercontractile State and Diastolic Failure in the α1CTG Mouse 英文参考文献.docVIP

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Dilated Cardiomyopathy with Increased SR Ca2+ Loading Preceded by a Hypercontractile State and Diastolic Failure in the α1CTG Mouse 英文参考文献.doc

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DilatedCardiomyopathywithIncreasedSRCa2LoadingPrecededbyaHypercontractileStateandDiastolicFailureintheα1CTGMouse英文参考文献

DilatedCardiomyopathywithIncreasedSRCa2+Loading PrecededbyaHypercontractileStateandDiastolic Failureinthea1CTGMouse SuWang1.,BruceZiman1.,IlonaBodi2.,MartaRubio2,Ying-YingZhou1¤,KarenD’Souza2,NanetteH. Bishopric3,ArnoldSchwartz2*,EdwardG.Lakatta1* 1LaboratoryofCardiovascularScience,GerontologyResearchCenter,NationalInstituteonAging,Baltimore,Maryland,UnitedStatesofAmerica,2InstituteofMolecular PharmacologyandBiophysics,DepartmentofSurgery,UniversityofCincinnati,CollegeofMedicine,Cincinnati,Ohio,UnitedStatesofAmerica,3DepartmentofMolecular andCellularPharmacology,MedicineandPediatrics,UniversityofMiamiMillerSchoolofMedicine,Miami,Florida,UnitedStatesofAmerica Abstract Miceover-expressingthea12subunit(pore)oftheL-typeCa2+channel(a1CTG)by4months(mo)ofageexhibitanenlarged heart, hypertrophied myocytes, increased Ca current and Ca2+ transient amplitude, but a normal SR Ca load. With advancingage(8–11mo),somemicedemonstrateadvancedhypertrophybutarenotincongestiveheartfailure(NFTG), while others evolve to frank dilated congestive heart failure (FTG). We demonstrate that older NFTG myocytes exhibit a hypercontractilestateoverawiderangeofstimulationfrequencies,butmaintainanormalSRCa2+loadcomparedtoage matchednon-transgenic(NTG)myocytes.However,athighstimulationrates(2–4Hz)signsofdiastoliccontractilefailure appearinNFTGcells.TheevolutionoffrankcongestivefailureinFTGisaccompaniedbyafurtherincreaseinheartmassand myocytesize,andphospholambanandryanodinereceptorproteinlevelsandphosphorylationbecomereduced.InFTG,the 2+ 2+ 2+ 2+ SR Ca load increases and Ca release following excitation, increases further. An enhanced NCX function in FTG, as reflectedbyanacceleratedrelaxationofthecaffeine-inducedCa transient,isinsufficienttomaintainanormaldiastolic 2+ 2+ during high rates of stimulation. Although a high SR Ca2+ release following excitation is maintained, the Ca hypercontractile state is not maintained at high rates of stimulation, and signs of both systolic and diastolic co