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Trypanosoma cruzi infection results in the reduced expression of caveolin-3 in the heart.
Adesse, Daniel; Lisanti, Michael P; Spray, David C; Machado, Fabiana S; Meirelles, Maria de Nazareth; Tanowitz, Herbert B; Garzoni, Luciana Ribeiro
Cell cycle (Georgetown, Tex.). 2010;9(8):1639-46.
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Abstract
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.