Key result
Treating cardiomyocytes with thapsigargin, which depletes intracellular calcium stores, resulted in a 75% inhibition of Trypanosoma cruzi invasion.
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Inhibition of SERCA with thapsigargin significantly reduces Trypanosoma cruzi invasion into cardiomyocytes, highlighting the role of intracellular calcium in the pathogenesis of Chagas cardiomyopathy.
The present paper summarizes new approaches regarding the progress done to the understanding of the interaction of Trypanosoma cruzi-cardiomyocytes. Mannose receptors localized at the surface of heart muscle cell are involved in binding and uptake of the parasite. One of the most striking events in the parasite-heart muscle cells interaction is the disruption of the actin cytoskeleton. We have investigated the regulation of the actin mRNA during the cytopathology induced in myocardial cells by the parasite. T. cruzi invasion increases calcium resting levels in cardiomyocytes. We have previously shown that Ca2+ ATPase of the sarcoplasmic reticulum (SERCA) is involved in the invasion of T. cruzi in cardiomyocytes. Treating the cells with thapsigargin, a drug that binds to all SERCA ATPases and causes depletion of intracellular calcium stores, we found a 75% inhibition in the T. cruzi-cardiomyocytes invasion.
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Meirelles et al. (1999) conducted a review in Trypanosoma cruzi infection. Thapsigargin was evaluated on T. cruzi-cardiomyocytes invasion (75% inhibition). Treating cardiomyocytes with thapsigargin, which depletes intracellular calcium stores, resulted in a 75% inhibition of Trypanosoma cruzi invasion.
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