Acyloxy Nitroso Compounds Inhibit LIF Signaling in Endothelial Cells and Cardiac Myocytes Evidence That STAT3 Signaling Is Redox-Sensitive 英文参考文献.docVIP

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Acyloxy Nitroso Compounds Inhibit LIF Signaling in Endothelial Cells and Cardiac Myocytes Evidence That STAT3 Signaling Is Redox-Sensitive 英文参考文献.doc

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Acyloxy Nitroso Compounds Inhibit LIF Signaling in Endothelial Cells and Cardiac Myocytes Evidence That STAT3 Signaling Is Redox-Sensitive 英文参考文献

AcyloxyNitrosoCompoundsInhibitLIFSignalingin EndothelialCellsandCardiacMyocytes:EvidenceThat STAT3SignalingIsRedox-Sensitive CarlosZgheib1,MazenKurdi2,FouadA.Zouein1,BarakW.Gunter1,BrianA.Stanley3,JoeZgheib4, DamianG.Romero5,S.BruceKing6,NazarenoPaolocci3,7,GeorgeW.Booz1* 1DepartmentsofPharmacologyandToxicology,SchoolofMedicine,andCenterforExcellenceinCardiovascular-RenalResearch,TheUniversityofMississippiMedical Center, Jackson,Mississippi, United States of America, 2Department ofChemistry and Biochemistry, Faculty of Sciences, Lebanese University, Rafic Hariri Educational Campus, Hadath, Lebanon, 3Division of Cardiology, Johns Hopkins Medical Institutions, Baltimore, Maryland, United States of America, 4Department of Medicine, Division of Cardiology, Centre Hospitalier Universitaire de Nancy, Brabois, France, 5Department of Biochemistry, School of Medicine, and Center for Excellence in Cardiovascular-Renal Research, The University of Mississippi Medical Center, Jackson, Mississippi, United States of America, 6Department of Chemistry, Wake Forest University,Winston-Salem,NorthCarolina,UnitedStatesofAmerica,7ClinicalMedicineDepartment,SectionofGeneralPathology,UniversityofPerugia,Perugia,Italy Abstract We previously showed that oxidative stress inhibits leukemia inhibitory factor (LIF) signaling by targeting JAK1, and the catalyticdomainsofJAK1and2haveacysteine-basedredoxswitch.Thus,wepostulatedthattheNOsiblingandthiophylic compound, nitroxyl (HNO), would inhibit LIF-induced JAK-STAT3 activation. Pretreatment of human microvascular endothelialcells(HMEC-1)orneonatalratcardiomyocyteswiththeHNOdonorsAngeli’ssaltornitrosocyclohexylacetate (NCA)inhibitedLIF-inducedSTAT3activation.NCApretreatmentalsoblockedtheinductionofdownstreaminflammatory genes (e.g. intercellular adhesion molecule 1, CCAAT/enhancer binding protein delta). The related 1-nitrosocyclohexyl pivalate(NCP;notanitroxyldonor)wasequallyeffectiveininhibitingSTAT3activation,suggestingthatthesecompounds actas