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- W1993327170 abstract "Recent studies using mice with genetically engineered gap junction protein connexin (Cx) genes have provided evidence that reduced gap-junctional coupling in ventricular cardiomyocytes predisposes to ventricular arrhythmia. However, the pathological processes of arrhythmogenesis due to abnormalities in gap junctions are poorly understood. We have postulated a hypothesis that dysfunction of gap junctions at the single-cell level may affect synchronization of calcium transients among cardiomyocytes. To examine this hypothesis, we developed a novel system in which gap-junctional intercellular communication in primary neonatal rat cardiomyocytes was inhibited by a mutated (Δ130–137) Cx43 fused with enhanced green fluorescent protein (Cx43–EGFP), and calcium transients were imaged in real time while the mutated Cx43–EGFP-expressing cardiomyocytes were identified. The mutated Cx43–EGFP inhibited dye coupling not only in the liver epithelial cell line IAR 20 but also in primary neonatal rat cardiomyocytes in a dominant-negative manner, whereas wild-type Cx43–EGFP made functional gap junctions in otherwise communication-deficient HeLa cells. The mutated Cx43–EGFP induced desynchronization of calcium transients among cardiomyocytes with significantly higher frequency than wild-type Cx43–EGFP. These results suggest that dysfunction of gap-junctional intercellular communication at the single-cell level could hamper synchronous beating among cardiomyocytes as a result of desynchronization of calcium transients." @default.
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- W1993327170 date "2002-02-01" @default.
- W1993327170 modified "2023-10-18" @default.
- W1993327170 title "Dominant-Negative Connexin43–EGFP Inhibits Calcium-Transient Synchronization of Primary Neonatal Rat Cardiomyocytes" @default.
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- W1993327170 doi "https://doi.org/10.1006/excr.2001.5411" @default.
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