| http://purl.uniprot.org/citations/23587598 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/23587598 | http://www.w3.org/2000/01/rdf-schema#comment | "Sustained β-adrenergic receptor stimulation is associated with cardiomyopathy, an affect thought to result from cAMP-associated cardiac injury. Using a murine line with adenylyl cyclase 6 gene deletion (AC6KO), we tested the hypothesis that AC6 deletion, by limiting cAMP production, would attenuate cardiomyopathy in the setting of sustained β-adrenergic receptor stimulation. During 7d isoproterenol infusion, there was unexpected higher mortality in AC6KO mice compared to wild type control mice (p<0.0001). However, left ventricular function was similarly impaired in isoproterenol-infused control and AC6KO mice. There were no group differences in left ventricular hypertrophy, apoptosis, and fibrosis. Telemetric electrocardiography showed progressive prolongation of PR interval (p<0.0001), QRS duration (p<0.0005), and QTc (p<0.0001), as well as reduction in heart rate (p<0.0001), in AC6KO mice during isoproterenol infusion. These defective electrophysiological properties in isoproterenol-infused AC6KO mice were associated with decreased longitudinal ventricular conduction velocity (p<0.05) and reduced phosphorylation of connexin 43 at S368 in left ventricular samples (p=0.006). Taken together, these data demonstrate that limiting cAMP production does not prevent sustained β-adrenergic receptor stimulation-induced cardiomyopathy. Moreover, AC6 deletion impairs electrophysiological properties and increases mortality during sustained β-adrenergic receptor stimulation. Decreased connexin 43 phosphorylation and impaired ventricular conduction may be of mechanistic importance for the defective electrophysiological properties."xsd:string |
| http://purl.uniprot.org/citations/23587598 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.yjmcc.2013.04.005"xsd:string |
| http://purl.uniprot.org/citations/23587598 | http://purl.uniprot.org/core/author | "Lee P."xsd:string |
| http://purl.uniprot.org/citations/23587598 | http://purl.uniprot.org/core/author | "Tang R."xsd:string |
| http://purl.uniprot.org/citations/23587598 | http://purl.uniprot.org/core/author | "Guo T."xsd:string |
| http://purl.uniprot.org/citations/23587598 | http://purl.uniprot.org/core/author | "Tang T."xsd:string |
| http://purl.uniprot.org/citations/23587598 | http://purl.uniprot.org/core/author | "Gao M.H."xsd:string |
| http://purl.uniprot.org/citations/23587598 | http://purl.uniprot.org/core/author | "Hammond H.K."xsd:string |
| http://purl.uniprot.org/citations/23587598 | http://purl.uniprot.org/core/author | "Lai N.C."xsd:string |
| http://purl.uniprot.org/citations/23587598 | http://purl.uniprot.org/core/author | "McCulloch A.D."xsd:string |
| http://purl.uniprot.org/citations/23587598 | http://purl.uniprot.org/core/author | "Wright A.T."xsd:string |
| http://purl.uniprot.org/citations/23587598 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
| http://purl.uniprot.org/citations/23587598 | http://purl.uniprot.org/core/name | "J Mol Cell Cardiol"xsd:string |
| http://purl.uniprot.org/citations/23587598 | http://purl.uniprot.org/core/pages | "60-67"xsd:string |
| http://purl.uniprot.org/citations/23587598 | http://purl.uniprot.org/core/title | "Adenylyl cyclase 6 deletion increases mortality during sustained beta-adrenergic receptor stimulation."xsd:string |
| http://purl.uniprot.org/citations/23587598 | http://purl.uniprot.org/core/volume | "60"xsd:string |
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