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Cardiovascular Research 2002 53(4):921-935; doi:10.1016/S0008-6363(01)00522-3
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

Redistribution of connexin45 in gap junctions of connexin43-deficient hearts

Carolyn M. Johnsona, Evelyn M. Kantera, Karen G. Greenb, James G. Laingc,1, Tetsuo Betsuyakua, Eric C. Beyerc,2, Thomas H. Steinberga, Jeffrey E. Saffitza,b,d and Kathryn A. Yamadaa,d,*

aDepartment of Medicine, Washington University School of Medicine, St. Louis, MO, USA
bDepartment of Pathology, Washington University School of Medicine, St. Louis, MO, USA
cDepartment of Pediatrics, Washington University School of Medicine, St. Louis, MO, USA
dCenter for Cardiovascular Research, Washington University School of Medicine, St. Louis, MO, USA

kyamada{at}im.wustl.edu

* Corresponding author. Cardiovascular Division, Box 8086, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA. Tel.: +1-314-3628-909; fax: +1-314-3628-957

Objective: Adult ventricular myocytes express two gap junction channel proteins: connexin43 (Cx43) and connexin45 (Cx45). Cx43-deficient mice exhibit slow ventricular epicardial conduction, suggesting that Cx43 plays an important role in intercellular coupling in the ventricle. Cx45 is much less abundant than Cx43 in working ventricular myocytes. Its role in ventricular conduction has not been defined, nor is it known whether expression or distribution of Cx45 is altered in Cx43-deficient mice. The present study was undertaken to determine (1) whether expression of Cx45 is upregulated and (2) whether gap junction structure and distribution are altered in Cx43-deficient mice. Methods: Ventricular tissue from neonatal Cx43+/+, Cx43+/– and Cx43–/– and adult Cx43+/+ and Cx43+/– mice was analyzed by immunoblotting and confocal immunofluorescence microscopy. Results: Total Cx45 protein abundance measured by immunoblotting was not different in Cx43-deficient or null hearts compared to wild-type control hearts. However, the amount and distribution of Cx45 immunoreactive signal measured by quantitative confocal analysis were markedly reduced in both Cx43+/– and Cx43–/– hearts. Conclusion: Although the total content of Cx45 is not upregulated in Cx43-deficient hearts, the localization of Cx45 to cardiac gap junctions depends on the expression level of Cx43 and is dramatically altered in mice that express no Cx43.

KEYWORDS Cell communication; Developmental biology; Gap junctions; Histo(patho)logy; Myocytes; Remodeling

1 Present address: Washington University School of Medicine, Infectious Diseases Division, Box 8051, St. Louis, MO 63110, USA.

2 Present address: The University of Chicago, Department of Pediatrics, Section of Hematology/Oncology, Chicago, IL 60637, USA.


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