Source:http://linkedlifedata.com/resource/pubmed/id/11795949
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2002-1-17
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| pubmed:abstractText |
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 (Delta130-137) 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.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Connexin 43,
http://linkedlifedata.com/resource/pubmed/chemical/Green Fluorescent Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Luminescent Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger
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| pubmed:status |
MEDLINE
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| pubmed:month |
Feb
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| pubmed:issn |
0014-4827
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| pubmed:author | |
| pubmed:copyrightInfo |
Copyright 2001 Elsevier Science.
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| pubmed:issnType |
Print
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| pubmed:day |
1
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| pubmed:volume |
273
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
85-94
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:11795949-Animals,
pubmed-meshheading:11795949-Animals, Newborn,
pubmed-meshheading:11795949-Calcium,
pubmed-meshheading:11795949-Cell Communication,
pubmed-meshheading:11795949-Cell Division,
pubmed-meshheading:11795949-Cells, Cultured,
pubmed-meshheading:11795949-Connexin 43,
pubmed-meshheading:11795949-Fluorescent Antibody Technique,
pubmed-meshheading:11795949-Gap Junctions,
pubmed-meshheading:11795949-Gene Expression,
pubmed-meshheading:11795949-Genes, Dominant,
pubmed-meshheading:11795949-Green Fluorescent Proteins,
pubmed-meshheading:11795949-HeLa Cells,
pubmed-meshheading:11795949-Humans,
pubmed-meshheading:11795949-Luminescent Proteins,
pubmed-meshheading:11795949-Mutation,
pubmed-meshheading:11795949-Myocardium,
pubmed-meshheading:11795949-RNA, Messenger,
pubmed-meshheading:11795949-Rats,
pubmed-meshheading:11795949-Rats, Wistar,
pubmed-meshheading:11795949-Signal Transduction,
pubmed-meshheading:11795949-Transfection
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| pubmed:year |
2002
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| pubmed:articleTitle |
Dominant-negative connexin43-EGFP inhibits calcium-transient synchronization of primary neonatal rat cardiomyocytes.
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| pubmed:affiliation |
Department of Pathology and Cell Regulation, Kyoto Prefectural University of Medicine, Kyoto, 602-8566, Japan.
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| pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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