ArticleCardiovascular research2010
Connexin43 knockdown or overexpression modulates cell coupling in control and failing rabbit left ventricular myocytes.
Article in Cardiovascular research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Changes in cardiac conduction time following cardiac resynchronization therapy: rationale and design of the RECOVER study.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2022Article
- Serine-threonine protein phosphatase regulation of Cx43 dephosphorylation in arrhythmogenic disorders.Cellular signalling · 2021Review
- Molecular remodeling of Cx43, but not structural remodeling, promotes arrhythmias in an arrhythmogenic canine model of nonischemic heart failure.Journal of molecular and cellular cardiology · 2021Article
- Alterations of housekeeping proteins in human aged and diseased hearts.Pflugers Archiv : European journal of physiology · 2021Article
- Ganglionated Plexi Ablation Suppresses Chronic Obstructive Sleep Apnea-Related Atrial Fibrillation by Inhibiting Cardiac Autonomic Hyperactivation.Frontiers in physiology · 2021Article
- Cardiac β-adrenergic receptor activation mediates distinct and cell type-dependent changes in the expression and distribution of connexin 43.Journal of cellular and molecular medicine · 2020Article
- Vascular smooth muscle cell phenotypic transition regulates gap junctions of cardiomyocyte.Heart and vessels · 2020Article
- Antiarrhythmic Mechanisms of Chinese Herbal Medicine Dingji Fumai Decoction.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- The stress kinase JNK regulates gap junction Cx43 gene expression and promotes atrial fibrillation in the aged heart.Journal of molecular and cellular cardiology · 2018Article
- Calcium-Dependent Arrhythmogenic Foci Created by Weakly Coupled Myocytes in the Failing Heart.Circulation research · 2017Article
- Connexins in Cardiovascular and Neurovascular Health and Disease: Pharmacological Implications.Pharmacological reviews · 2017Review
- Regulation of cardiac gap junctions by protein phosphatases.Journal of molecular and cellular cardiology · 2017Review
- Cdon deficiency causes cardiac remodeling through hyperactivation of WNT/β-catenin signaling.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Involvement of Rictor/mTORC2 in cardiomyocyte differentiation of mouse embryonic stem cellsInternational journal of biological sciences · 2017Article
- Connexin 43 is an emerging therapeutic target in ischemia/reperfusion injury, cardioprotection and neuroprotection.Pharmacology & therapeutics · 2015Review
- Article
- c-Jun N-terminal kinase activation contributes to reduced connexin43 and development of atrial arrhythmias.Cardiovascular research · 2013Article
- Regulatory effect of connexin 43 on basal Ca2+ signaling in rat ventricular myocytes.PloS one · 2012Article
- Enhanced activation of p21-activated kinase 1 in heart failure contributes to dephosphorylation of connexin 43.Cardiovascular research · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
aimsWe have shown that failing human and rabbit left ventricle (LV) exhibits downregulation and dephosphorylation of connexin43 (Cx43) and that Cx43 dephosphorylation in heart failure (HF) contributes to reduced cell coupling. However, the role of Cx43 downregulation per se in impaired coupling in HF is unclear. METHODS AND
resultsFirst, we used adenovirus (Ad) encoding a Cx43 siRNA sequence to knock down Cx43 protein levels in cultured control rabbit LV myocytes. Cells cultured for up to 48 h with intermittent pacing maintained Cx43 protein levels and phosphorylation status. Cell coupling in Cx43 knockdown myocyte pairs (by Lucifer Yellow dye transfer) was markedly reduced after 24 h infection (associated with approximately 40% Cx43 knockdown) and after 48 h (associated with approximately 70% Cx43 knockdown). The phosphorylation status, distribution of remaining Cx43 proteins, and levels of other cardiac connexins (Cx40 and Cx45) were unchanged. Second, we overexpressed Cx43 to levels comparable to control using an adenovirus encoding wild-type Cx43 (Cx43WT) gene in isolated LV myocytes from our arrhythmogenic HF rabbit model. We found 87% more Cx43WT proteins improved dye coupling [vs. Ad-beta-galactosidase (LacZ) infected HF controls]. Overexpressed Cx43 protein was located throughout the myocyte membrane (same pattern as in controls), and the phosphorylation status of Cx43 remained comparable to that in AdLacZ infected HF controls.
conclusionIn addition to Cx43 dephosphorylation, downregulation of Cx43 plays an essential role in reduced cell coupling in the failing rabbit heart. Modulation of Cx43 expression could be a novel therapeutic approach to improve conduction and decrease sudden death in HF.
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