http://purl.uniprot.org/citations/21195051 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/21195051 | http://www.w3.org/2000/01/rdf-schema#comment | "Background and objectiveCardiac-directed adenylyl cyclase 6 (AC6) expression attenuates left ventricular (LV) hypertrophy and dysfunction in cardiomyopathy, but its effects in the pressure-overloaded heart are unknown.MethodsMice with cardiac-directed and regulated expression of AC6 underwent transaortic constriction (TAC) to induce LV pressure overload. Ten days prior to TAC, and for the duration of the 4 week study, cardiac myocyte AC6 expression was activated in one group (AC-On) but not the other (AC-Off). Multiple measures of LV systolic and diastolic function were obtained 4 weeks after TAC, and LV samples assessed for alterations in Ca2+ signaling.ResultsLV contractility, as reflected in the end-systolic pressure-volume relationship (Emax), was increased (p=0.01) by activation of AC6 expression. In addition, diastolic function was improved (p<0.05) and LV dilation was reduced (p<0.05). LV samples from AC-On mice showed reduced protein expression of sodium/calcium exchanger (NCX1) (p<0.05), protein phosphatase 1 (PP1) (p<0.01), and increased phosphorylation of phospholamban (PLN) at Ser16 (p<0.05). Finally, sarcoplasmic reticulum (SR) Ca2+ content was increased in cardiac myocytes isolated from AC-On mice (p<0.05).ConclusionsActivation of cardiac AC6 expression improves function of the pressure-overloaded and failing heart. The predominant mechanism for this favorable adaptation is improved Ca2+ handling, a consequence of increased PLN phosphorylation, reduced NCX1, reduced PP1 expression, and increased SR Ca2+ content."xsd:string |
http://purl.uniprot.org/citations/21195051 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.bbrc.2010.12.113"xsd:string |
http://purl.uniprot.org/citations/21195051 | http://purl.uniprot.org/core/author | "Sugano Y."xsd:string |
http://purl.uniprot.org/citations/21195051 | http://purl.uniprot.org/core/author | "Firth A.L."xsd:string |
http://purl.uniprot.org/citations/21195051 | http://purl.uniprot.org/core/author | "Gao M.H."xsd:string |
http://purl.uniprot.org/citations/21195051 | http://purl.uniprot.org/core/author | "Hammond H.K."xsd:string |
http://purl.uniprot.org/citations/21195051 | http://purl.uniprot.org/core/author | "Lai N.C."xsd:string |
http://purl.uniprot.org/citations/21195051 | http://purl.uniprot.org/core/author | "Yuan J.X."xsd:string |
http://purl.uniprot.org/citations/21195051 | http://purl.uniprot.org/core/author | "Lew W.Y."xsd:string |
http://purl.uniprot.org/citations/21195051 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
http://purl.uniprot.org/citations/21195051 | http://purl.uniprot.org/core/name | "Biochem Biophys Res Commun"xsd:string |
http://purl.uniprot.org/citations/21195051 | http://purl.uniprot.org/core/pages | "349-355"xsd:string |
http://purl.uniprot.org/citations/21195051 | http://purl.uniprot.org/core/title | "Activated expression of cardiac adenylyl cyclase 6 reduces dilation and dysfunction of the pressure-overloaded heart."xsd:string |
http://purl.uniprot.org/citations/21195051 | http://purl.uniprot.org/core/volume | "405"xsd:string |
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