Chagas disease, which is caused by the intracellular protozoan
Trypanosoma cruzi
, is a serious health problem
in Latin America. The heart is one of the major organs affected by this parasitic infection. The pathogenesis
of tissue remodelling, particularly regarding cardiomyocyte behaviour after parasite infection, and the molecular
mechanisms that occur immediately following parasite entry into host cells are not yet completely understood.
Previous studies have reported that the establishment of parasitism is connected to the activation of the phosphatidylinositol-
3 kinase (PI3K), which controls important steps in cellular metabolism by regulating the production
of the second messenger phosphatidylinositol-3,4,5-trisphosphate. Particularly, the tumour suppressor PTEN
is a negative regulator of PI3K signalling. However, mechanistic details of the modulatory activity of PTEN on
Chagas disease have not been elucidated. To address this question, H9c2 cells were infected with
T. cruzi Berenice
62 strain and the expression of a specific set of microRNAs (miRNAs) were investigated. Our cellular model
demonstrated that miRNA-190b is correlated to the decrease of cellular viability rates by negatively modulating
PTEN protein expression in
T. cruzi-infected cells.
