Trypanosoma cruzi induces changes in cardiac connexin43 expression

Daniel Adesse, Luciana R. Garzoni, Huan Huang, Herbert B. Tanowitz, Maria de Nazareth Meirelles, David C. Spray

Research output: Contribution to journalArticle

21 Scopus citations

Abstract

Gap junction proteins (connexins) are required for myocardial function, since they allow intercellular transmission of current carrying ions and signaling molecules. Previous studies demonstrated that rat cardiac myocytes infected with Trypanosoma cruzi lost gap junctional communication and decreased automaticity. We infected mouse cardiac myocytes with trypomastigotes of the Y strain of T. cruzi and observed alterations in connexin43 (Cx43) distribution. One hour post infection Cx43 levels were significantly increased. However, at longer time points post infection there was a significant loss of Cx43 staining in membranes of infected cardiac myocytes. Interestingly, there was also a significant reduction in myocardial Cx43 protein levels during acute infection. These data indicate that T. cruzi infection alters Cx43 expression both in vitro and in vivo. Disruptions in Cx43 may contribute to the pathogenesis of cardiac electrical alterations observed in T. cruzi infection.

Original languageEnglish (US)
Pages (from-to)21-28
Number of pages8
JournalMicrobes and Infection
Volume10
Issue number1
DOIs
Publication statusPublished - Jan 1 2008

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Keywords

  • Cardiac myocytes
  • Chagas' disease
  • Connexin43
  • Gap junctions
  • Trypanosoma cruzi

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Infectious Diseases

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