Trypanosoma cruzi infection disrupts vinculin costameres in cardiomyocytes

• Published in: European journal of cell biology 2004-10, Vol.83 (10), p.531-540
• Main Authors: Melo, Tatiana G., Almeida, Danielle S., de Nazareth, Maria, de Meirelles, S.L., Pereira, Mirian Claudia S.
• Format: Article
• Language: English
• Subjects: Animals; Cardiomyocytes; Cell Membrane - ultrastructure; Cells, Cultured; Chagas Cardiomyopathy - parasitology; Chagas Cardiomyopathy - pathology; Chagas Cardiomyopathy - physiopathology; Disease Models, Animal; Disease Progression; Fluorescent Antibody Technique, Indirect; Focal adhesion protein; Gene Expression; Heart - parasitology; Host-Parasite Interactions; Immunoblotting; Male; Mice; Microscopy, Fluorescence; Myocardium - metabolism; Myocardium - ultrastructure; Myocytes, Cardiac - metabolism; Myocytes, Cardiac - parasitology; Myocytes, Cardiac - ultrastructure; Myofibrils - metabolism; Myofibrils - ultrastructure; Trypanosoma cruzi; Trypanosoma cruzi - pathogenicity; Vinculin; Vinculin - metabolism
• ISSN: 0171-9335; 1618-1298
• DOI: 10.1078/0171-9335-00419

Chagas' disease cardiomyopathy is an important manifestation of Trypanosoma cruzi infection, leading to cardiac dysfunction and serious arrhythmias. We have here investigated by indirect immunofluorescence assay the distribution of vinculin, a focal adhesion protein with a major role in the transmission of contraction force, during the T. cruzi-cardiomyocyte infection in vitro and in vivo. No change in vinculin distribution was observed after 24 h of infection, where control and T. cruzi-infected cardiomyocytes displayed vinculin localized at costameres and intercalated discs. On the other hand, a clear disruption of vinculin costameric distribution was noted after 72 h of infection. A significant reduction in the levels of vinculin expression was observed at all times of infection. In murine experimental Chagas' disease, alteration in the vinculin distribution was also detected in the infected myocardium, with no costameric staining in infected myocytes and irregular alignment of intercalated discs in cardiac fibers. These data suggest that the disruption of costameric vinculin distribution and the enlargement of interstitial space due to inflammatory infiltration may contribute to the reduction of transmission of cardiac contraction force, leading to alterations in the heart function in Chagas' disease.