Gene Transfer of Connexin43 Mutants Attenuates Coupling in Cardiomyocytes

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Gene transfer of connexin43 mutants attenuates coupling in cardiomyocytes: novel basis for modulation of cardiac conduction by gene therapy.

Modification of electrical conduction would be a useful principle to recruit in preventing or treating certain arrhythmias, notably ventricular tachycardia (VT). Here we pursue a novel gene transfer approach to modulate electrical conduction by reducing gap junctional intercellular communication (GJIC) and hence potentially modify the arrhythmia substrate. The ultimate goal is to develop a nond...

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Gene transfer of connexin43 into skeletal muscle.

Cellular cardiomyoplasty using skeletal myoblasts may be beneficial for infarct repair. One drawback to skeletal muscle cells is their lack of gap junction expression after differentiation, thus preventing electrical coupling to host cardiomyocytes. We sought to overexpress the gap junction protein connexin43 (Cx43) in differentiated skeletal myotubes, using retroviral, adenoviral, and plasmid-...

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Connexin43 gene transfer reduces ventricular tachycardia susceptibility after myocardial infarction.

OBJECTIVES The aim of this study was to evaluate the links between connexin43 (Cx43) expression, myocardial conduction velocity, and ventricular tachycardia in a model of healed myocardial infarction. BACKGROUND Post-infarction ventricular arrhythmias frequently cause sudden death. Impaired myocardial conduction has previously been linked to ventricular arrhythmias. Altered connexin expressio...

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Decreased efficiency of adenovirus-mediated gene transfer in aging cardiomyocytes.

BACKGROUND Aging is an independent risk factor for the development of cardiovascular disease. Clinical application of myocardial gene transfer may be best suited in the elderly. In vivo gene transfer by adenovirus is less efficient in aging myocardium. METHODS AND RESULTS When infected with adenovirus containing beta-galactosidase (beta-gal) and green fluorescent protein (GFP) driven by cytom...

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Amphetamine activates connexin43 gene expression in cultured neonatal rat cardiomyocytes through JNK and AP-1 pathway.

OBJECTIVE Amphetamine has been known to induce cardiac dysrhythmia and sudden death. However, the molecular mechanism for the induction of dysrhythmia is not known. Connexin43 (Cx43) plays an important role for arrhythmogenesis. This study was undertaken to test the hypothesis that amphetamine could induce Cx43 expression in cardiac myocytes. METHODS Neonatal Wistar rat cardiac myocytes were ...

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ژورنال

عنوان ژورنال: Circulation Research

سال: 2007

ISSN: 0009-7330,1524-4571

DOI: 10.1161/circresaha.106.144956