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- IOC - Artigos de Periódicos [12642]
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THE INVOLVEMENT OF FAK AND SRC IN THE INVASION OF CARDIOMYOCYTES BY TRYPANOSOMA CRUZI
Autor
Afiliación
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Ultra-estrutura Celular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Ultra-estrutura Celular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Ultra-estrutura Celular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Ultra-estrutura Celular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Ultra-estrutura Celular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Ultra-estrutura Celular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Ultra-estrutura Celular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Ultra-estrutura Celular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Ultra-estrutura Celular. Rio de Janeiro, RJ, Brasil.
Resumen en ingles
The activation of signaling pathways involving protein tyrosine kinases (PTKs) has been demonstrated
during Trypanosoma cruzi invasion. Herein, we describe the participation of FAK/Src in the invasion of
cardiomyocytes by T. cruzi. The treatment of cardiomyocytes with genistein, a PTK inhibitor, significantly
reduced T. cruzi invasion. Also, PP1, a potent Src-family protein inhibitor, and PF573228, a specific FAK
inhibitor, also inhibited T. cruzi entry; maximal inhibition was achieved at concentrations of 25 lM
PP1 (53% inhibition) and 40 lM PF573228 (50% inhibition). The suppression of FAK expression in siRNA-
treated cells and tetracycline-uninduced Tet-FAK(WT)-46 cells significantly reduced T. cruzi invasion.
The entry of T. cruzi is accompanied by changes in FAK and c-Src expression and phosphorylation. An
enhancement of FAK activation occurs during the initial stages of T. cruzi-cardiomyocyte interaction
(30 and 60 min), with a concomitant increase in the level of c-Src expression and phosphorylation,
suggesting that FAK/Src act as an integrated signaling pathway that coordinates parasite entry. These
data provide novel insights into the signaling pathways that are involved in cardiomyocyte invasion
by T. cruzi. A better understanding of the signal transduction networks involved in T. cruzi invasion
may contribute to the development of more effective therapies for the treatment of Chagas’ disease.
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