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dc.contributor.authorChou, Chung-Chuanen_US
dc.contributor.authorHo, Chien-Teen_US
dc.contributor.authorLee, Hui-Lingen_US
dc.contributor.authorChu, Yenen_US
dc.contributor.authorYen, Tzung-Haien_US
dc.contributor.authorWen, Ming-Shienen_US
dc.contributor.authorLin, Shien-Fongen_US
dc.contributor.authorLee, Cheng-Hungen_US
dc.contributor.authorChang, Po-Chengen_US
dc.date.accessioned2018-08-21T05:52:47Z-
dc.date.available2018-08-21T05:52:47Z-
dc.date.issued2017-10-01en_US
dc.identifier.issn0147-8389en_US
dc.identifier.urihttp://dx.doi.org/10.1111/pace.13166en_US
dc.identifier.urihttp://hdl.handle.net/11536/143956-
dc.description.abstractBackgroundDiabetes mellitus is associated an increased risk of ventricular arrhythmias (VAs), but the underlying electrophysiological mechanisms are not fully explored. This study was aimed to test whether dynamic factors and Ca-i handling play roles in arrhythmogenesis of a diabetic animal model. Methods: We used 26 db/db type 2 diabetes mice and 28 control mice in this study. VA inducibility was evaluated in vivo under isoflurane general anesthesia. The intracellular Ca2+ (Ca-i) and membrane voltage (V-m) signals of the Langendorff-perfused mouse hearts were simultaneously recorded using the optical mapping technique. Action potential duration (APD), Ca-i dynamics conduction velocity (CV), and arrhythmogenic alternans were analyzed. Western blot was conducted to examine expressions of calcium handling and associated ion channels proteins. Results: The diabetic db/db mice showed significantly increased VA inducibility and severity. Longer APD and Ca-i transient duration and slower Ca-i decay and CV in the db/db mice than these in the control ones were observed. Dynamic pacing showed increased incidence of spatially discordant alternans leading to more VA inducibility in the db/db mice. Western blot analyses revealed increased phosphorylated-Ca2+/calmodulin-dependent protein kinase II protein expression and decreased ryanodine receptor protein expression, which probably underlay the molecular mechanisms of enhanced arrhythmogenicity in db/db mice. Conclusions: The type 2 diabetic mouse hearts show impaired repolarization, Ca-i handling homeostasis, and cardiac conduction reserve, leading to vulnerability of spatially discordant alternans development and induction of VA. Altered Ca-i-handling protein expressions probably underlie the molecular mechanisms of arrhythmogenicity in the type 2 diabetes animal model.en_US
dc.language.isoen_USen_US
dc.subjectarrhythmiaen_US
dc.subjectconduction velocityen_US
dc.subjectdb/db mouseen_US
dc.subjectintracellular calcium dynamicsen_US
dc.subjecttype 2 diabetesen_US
dc.titleRoles of impaired intracellular calcium cycling in arrhythmogenicity of diabetic mouse modelen_US
dc.typeArticleen_US
dc.identifier.doi10.1111/pace.13166en_US
dc.identifier.journalPACE-PACING AND CLINICAL ELECTROPHYSIOLOGYen_US
dc.citation.volume40en_US
dc.citation.spage1087en_US
dc.citation.epage1095en_US
dc.contributor.department分子醫學與生物工程研究所zh_TW
dc.contributor.departmentInstitute of Molecular Medicine and Bioengineeringen_US
dc.identifier.wosnumberWOS:000413353200008en_US
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