Document Detail


Cell-to-cell interaction prevents cell death in cultured neonatal rat ventricular myocytes.
MedLine Citation:
PMID:  11033109     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: Loss of cardiac cells and the anatomical or functional remodeling of intercellular coupling occur under several pathological conditions. We have assessed the significance of intercellular coupling for cell death. METHODS AND RESULTS: Ventricular cells obtained from 1 day old Wistar rats were cultured. Apoptosis was detected by nick-end labeling. Cells were plated at low and high cell density (3x10(4)/ml and 12x10(4)/ml, respectively). Cultured myocytes died spontaneously by apoptosis in a time dependent manner. The increase of the apoptotic cell population in a culture with high cell density on day 4 (1+/-1.2%, n=4) was significantly lower than that in a culture with low cell density (20+/-5.5%, n=4). The progression of apoptosis in the culture of low cell density was prevented in part after application of the medium extract from the culture of high cell density; the apoptotic cell population on day 6 decreased from 57+/-8.0% (n=4) to 36+/-3.8% (n=4). Treatment of the cultured myocytes at high cell density with antisense oligonucleotide for connexin43 (Cx43) for 24 h on day 2 resulted in a significant decrease in Cx43 expression as judged by Western blot, dye transfer and immunocytochemistry using mouse monoclonal antibody for Cx43. In association with the down-regulation of Cx43, the progress of apoptosis was accelerated; the apoptotic cell population on day 5 in the antisense-treated cultures (27+/-5.7%, n=4) was significantly higher than the sense-treated cultures (5+/-1.1%, n=4). The effect of Cx43 antisense treatment to promote apoptosis was not reversed by application of high cell-density culture medium. CONCLUSIONS: These findings suggest that cell-cell communication through gap junction formation and some humoral factors play important roles in the survival of cultured myocytes.
Authors:
K Yasui; K Kada; M Hojo; J K Lee; K Kamiya; J Toyama; T Opthof; I Kodama
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cardiovascular research     Volume:  48     ISSN:  0008-6363     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  2000 Oct 
Date Detail:
Created Date:  2000-11-20     Completed Date:  2000-11-20     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  68-76     Citation Subset:  IM    
Affiliation:
Department of Circulation, Division of Organ Function, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan.
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MeSH Terms
Descriptor/Qualifier:
Actinin / analysis
Animals
Animals, Newborn
Apoptosis / physiology*
Blotting, Western
Cell Communication
Cells, Cultured
Connexin 43 / analysis
Gap Junctions / physiology*
Immunohistochemistry
In Situ Nick-End Labeling
Mice
Myocardium / cytology,  metabolism*
Oligonucleotides, Antisense / pharmacology
Rats
Rats, Wistar
Time Factors
Chemical
Reg. No./Substance:
0/Connexin 43; 0/Oligonucleotides, Antisense; 11003-00-2/Actinin
Comments/Corrections
Comment In:
Cardiovasc Res. 2000 Oct;48(1):8-10   [PMID:  11033102 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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