Trypanosoma cruzi infection results in the reduced expression of caveolin-3 in the heart

• Published in: Cell cycle (Georgetown, Tex.) Tex.), 2010-04, Vol.9 (8), p.1639-1646
• Main Authors: Adesse, Daniel, Lisanti, Michael P., Spray, David C., Machado, Fabiana S., de Nazareth Meirelles, Maria, Tanowitz, Herbert B., Garzoni, Luciana Ribeiro
• Format: Article
• Language: English
• Subjects: Animals; Binding; Biology; Bioscience; Calcium; Cancer; Caveolae - metabolism; Caveolin 3 - metabolism; Cell; Chagas Disease - metabolism; Cycle; Landes; Mice; Mice, Knockout; Mitogen-Activated Protein Kinase 1 - metabolism; Mitogen-Activated Protein Kinase 3 - metabolism; Myocytes, Cardiac - metabolism; Myocytes, Cardiac - parasitology; Myocytes, Cardiac - ultrastructure; Organogenesis; Proteins; Trypanosoma cruzi
• ISSN: 1538-4101; 1551-4005
• DOI: 10.4161/cc.9.8.11509

Caveolae are motile, membrane-bound compartments that contain a number of molecules that participate in cell signaling. Caveolins are protein markers of caveolae and function in a variety of biological processes. Caveolin-3 (Cav-3) is expressed in muscle cells and Cav-3 null mice display a cardiomyopathic phenotype. Ultrastructural cytochemistry, confocal microscopy and immunoblotting revealed a reduction in Cav-3 expression and an activation of ERK (extracellular-signal-regulated kinase) 48 hours after Trypanosoma cruzi infection of cultured cardiac myocytes. CD-1 mice infected with the Brazil strain of T. cruzi displayed reduced expression of Cav-3 and activation of ERK 66 days post infection (dpi).   By 180 dpi there was a normalization of these values. These data suggest that the reduction in Cav-3 expression and the activation of ERK during the early phase of infection may contribute to the pathogenesis of chagasic cardiomyopathy.