Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2003 Jan;242(1-2):135-44.

Gap junction remodeling and altered connexin43 expression in the failing human heart

Sawa Kostin  1 , Markus Rieger, Sebastian Dammer, Stefan Hein, Manfred Richter, Wölf-Peter Klövekorn, Erwin P Bauer, Jutta Schaper
Affiliations
  • PMID: 12619876

Gap junction remodeling and altered connexin43 expression in the failing human heart

Sawa Kostin et al. Mol Cell Biochem. 2003 Jan.

Abstract

Gap junctions (GJ) are important determinants of cardiac conduction and the evidence has recently emerged that altered distribution of these junctions and changes in the expression of their constituent connexins (Cx) may lead to abnormal coupling between cardiomyocytes and likely contribute to arrhythmogenesis. However, it is largely unknown whether changes in the expression and distribution of the major cardiac GJ protein, Cx43, is a general feature of diverse chronic myocardial diseases or is confined to some particular pathophysiological settings. In the present study, we therefore set out to investigate qualitatively and quantitatively the distribution and expression of Cx43 in normal human myocardium and in patients with dilated (DCM), ischemic (ICM), and inflammatory cardiomyopathies (MYO). Left ventricular tissue samples were obtained at the time of cardiac transplantation and investigated with immunoconfocal and electron microscopy. As compared with the control group, Cx43 labeling in myocytes bordering regions of healed myocardial infarction (ICM), small areas of replacement fibrosis (DCM) and myocardial inflammation (MYO) was found to be highly disrupted instead of being confined to the intercalated discs. In all groups, myocardium distant from these regions showed an apparently normal Cx43 distribution at the intercalated discs. Quantitative immunoconfocal analysis of Cx43 in the latter myocytes revealed that the Cx43 area per myocyte area or per myocyte volume is significantly decreased by respectively 30 and 55% in DCM, 23 and 48% in ICM, and by 21 and 40% in MYO as compared with normal human myocardium. In conclusion, focal disorganization of GJ distribution and down-regulation of Cx43 are typical features of myocardial remodeling that may play an important role in the development of an arrhythmogenic substrate in human cardiomyopathies.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Circulation. 1981 Apr;63(4):882-94 - PubMed
    1. Bioessays. 1996 Sep;18(9):719-30 - PubMed
    1. J Mol Cell Cardiol. 2001 Feb;33(2):359-71 - PubMed
    1. Microsc Res Tech. 2001 Feb 1;52(3):301-22 - PubMed
    1. J Clin Invest. 1997 Apr 15;99(8):1991-8 - PubMed

LinkOut - more resources