Loss of Plakophilin-2 Expression Leads to Decreased Sodium Current and Slower Conduction Velocity in Cultured Cardiac Myocytes
| Autor: | Lori L. Isom, Guadalupe Guerrero-Serna, Wanda Coombs, Mario Delmar, Hassan Hussein Musa, Priscila Y. Sato, Steven M. Taffet, Gustavo Patino |
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| Rok vydání: | 2009 |
| Předmět: |
medicine.medical_specialty
genetic structures Action potential Physiology Sodium Action Potentials chemistry.chemical_element NAV1.5 Voltage-Gated Sodium Channel Biology Sodium Channels Article Rats Sprague-Dawley Desmosome Internal medicine Ventricular Dysfunction medicine Animals Myocyte Myocytes Cardiac Patch clamp Sodium channel Arrhythmias Cardiac Desmosomes Rats medicine.anatomical_structure Endocrinology Gene Expression Regulation chemistry Gene Knockdown Techniques Biophysics Cardiomyopathies Cardiology and Cardiovascular Medicine Intercalated disc Plakophilins |
| Zdroj: | Circulation Research. 105:523-526 |
| ISSN: | 1524-4571 0009-7330 |
| DOI: | 10.1161/circresaha.109.201418 |
| Popis: | Rationale: Plakophilin-2 (PKP2) is an essential component of the cardiac desmosome. Recent data show that it interacts with other molecules of the intercalated disc. Separate studies show preferential localization of the voltage-gated sodium channel (Na V 1.5) to this region. Objective: To establish the association of PKP2 with sodium channels and its role on action potential propagation. Methods and Results: Biochemical, patch clamp, and optical mapping experiments demonstrate that PKP2 associates with Na V 1.5, and that knockdown of PKP2 expression alters the properties of the sodium current, and the velocity of action potential propagation in cultured cardiomyocytes. Conclusions: These results emphasize the importance of intermolecular interactions between proteins relevant to mechanical junctions, and those involved in electric synchrony. Possible relevance to the pathogenesis of arrhythmogenic right ventricular cardiomyopathy is discussed. |
| Databáze: | OpenAIRE |
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