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Cyclin and Caveolin Expression in an Acute Model of Murine Chagasic Myocarditis

Fnu Nagajyothi, Mahalia Desruisseaux, Boumediene Bouzahzah, Louis M. Weiss, Daniele dos Santos Andrade, Stephen M. Factor, Philipp E. Scherer, Chris Albanese, Michael P. Lisanti and Herbert B. Tanowitz

volume 5 | issue 1

1 january 2006
Pages: 107 - 112

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Chagas’ disease caused by the parasite, Trypanosoma cruzi, is accompanied by an acute myocarditis which can be fatal. Mice (A/J strain) infected with T. cruzi (Tulahuern strain) develop an acute myocarditis associated with high parasitemia and uniform mortality. Examination of the myocardium demonstrated myonecrosis, vasculitis and parasite pseudocysts. Immunoblot analysis and quantitative real time PCR of heart lysates demonstrated an increased expression of cell cycle regulatory proteins such as cyclins B1, D1, A1 and E1 and an increased expression of cdk2 when compared with uninfected controls. Extracellular signal-regulated kinase (ERK) was activated. Proliferating cell nuclear antigen (PCNA), endothelin-1, endothelin receptor type A (ETA) and endothelin receptor type B (ETB) expression were increased. Caveolin-1 is important in the regulation of ERK and cyclin D1. The expression of caveolin-1 as well as caveolin-2 and caveolin-3 was reduced. These data suggest that acute fatal T. cruzi myocarditis is accompanied by changes in cell cycle proteins such as the cyclins and caveolin and the upregulation of the endothelin pathway which may be important in the myocardial abnormalities and the mortality observed in this mouse model.



We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
 Download PDF

If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.