Trypanosoma cruzi induces changes in cardiac connexin43 expression.
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.
Adesse
Daniel
D
Laboratorio de Ultra-estrutura Celular, Instituto Oswaldo Cruz - Fiocruz, Rio de Janeiro, Brazil.
Garzoni
Luciana R
LR
Huang
Huan
H
Tanowitz
Herbert B
HB
de Nazareth Meirelles
Maria
M
Spray
David C
DC
D000818:Animals; D002478:Cells, Cultured; D018031:Connexin 43 / Q000378:metabolism*; D051379:Mice; D008856:Microscopy, Fluorescence; D009206:Myocardium / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000469:parasitology*; D014349:Trypanosoma cruzi / Q000502:physiology*
D018031:Connexin 43