Anthrax Lethal Toxin Suppresses Murine Cardiomyocyte Contractile Function and Intracellular Ca2+ Handling via a NADPH Oxidase-Dependent Mechanism 英文参考文献.docVIP
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AnthraxLethalToxinSuppressesMurineCardiomyocyteContractileFunctionandIntracellularCa2HandlingviaaNADPHOxidase-DependentMechanism英文参考文献
AnthraxLethalToxinSuppressesMurineCardiomyocyte
ContractileFunctionandIntracellularCa Handlingviaa
NADPHOxidase-DependentMechanism
2+
MachenderR.Kandadi1,YinanHua1,HengMa1,QunLi1,Shu-ruKuo2,ArthurE.Frankel2,JunRen1*
1CenterforCardiovascularResearchandAlternativeMedicine,UniversityofWyomingCollegeofHealthSciences,Laramie,Wyoming,UnitedStatesofAmerica,2Cancer
ResearchInstituteofScottandWhiteMemorialHospital,Temple,Texas,UnitedStatesofAmerica
Abstract
Objectives:Anthraxinfectionisassociatedwithdevastatingcardiovascularsequelae,suggestingunfavorablecardiovascular
effectsoftoxinsoriginatedfromBacillusanthracisnamelylethalandedematoxins.Thisstudywasdesignedtoexaminethe
directeffectoflethaltoxinsoncardiomyocytecontractileandintracellularCa2+
properties.
Methods: Murine cardiomyocyte contractile function and intracellular Ca2+ handling were evaluated including peak
shortening (PS), maximal velocity of shortening/ relengthening (6 dL/dt), time-to-PS (TPS), time-to-90% relengthening
(TR90),intracellularCa risemeasuredasfura-2fluorescentintensity(DFFI),andintracellularCa2+decayrate.Stresssignaling
2+
2+
andCa regulatoryproteinswereassessedusingWesternblotanalysis.
Results:Invitroexposuretoalethaltoxin(0.05–50nM)elicitedaconcentration-dependentdepressiononcardiomyocyte
contractileandintracellularCa properties(PS,6dL/dt,DFFI),alongwithprolongeddurationofcontractionandintracellular
2+
2+
Ca
decay, the effects of which were nullified by the NADPH oxidase inhibitor apocynin. The lethal toxin significantly
enhanced superoxide production and cell death, which were reversed by apocynin. In vivo lethal toxinexposure exerted
similartime-dependentcardiomyocytemechanicalandintracellularCa2+responses.StresssignalingcascadesincludingMEK1/
2,p38,ERKandJNKwereunaffectedbyinvitrolethaltoxinswhereastheyweresignificantlyalteredbyinvivolethaltoxins.
2+
Ca regulatoryproteinsSERCA2aandphospholambanwerealsodifferentiallyregulatedbyinvitroandinvivolethaltoxins.
Autophagywasdrasticallytriggered
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