Natural programmed cell death in T. cruzi epimastigotes maintained in axenic cultures
Authors:
- 30 July 2008
- journal article
- research article
- Published by Wiley in Journal of Cellular Biochemistry
- Vol. 105 (3) , 688-698
Abstract
Trypanosoma cruzi, a parasitic protozoan, is the agent of Chagas' disease or American trypanosomiasis, an endemic pathology in Latin America, affecting up to 18 million people, with high public health costs. Programmed cell death (PCD) has many functions in development and tissue remodeling in metazoans. In protozoa, it could represent concomitant or alternative mechanisms for clonal selection, immune response evasion, and population size regulation. In this work, we describe the natural occurrence of PCD in T. cruzi epimastigotes during the stationary phase of growth in axenic culture or under nutrient deprivation. Thus, we have observed phosphatidylserine externalization, cellular volume decrease, caspase‐like protein activity, and DNA fragmentation. Additionally, serum deprivation also induces autophagic characteristics such as monodansylcadaverine‐labeled vesicles accumulation and redistribution of proteins homologous to Atg8. In agreement with our results, apoptosis may play an important role in parasite survival. Then, identification and modulation of molecular targets inducing programmed cell death in T. cruzi may lead to new potential therapeutic approaches for Chagas' disease. J. Cell. Biochem. 105: 688–698, 2008.Keywords
This publication has 53 references indexed in Scilit:
- Protein turnover and differentiation in LeishmaniaInternational Journal for Parasitology, 2007
- Developmental apoptosis in C. elegans: a complex CEDnarioNature Reviews Molecular Cell Biology, 2006
- Prostaglandin D2 induces programmed cell death in Trypanosoma brucei bloodstream formCell Death & Differentiation, 2005
- Paraptosis: mediation by MAP kinases and inhibition by AIP-1/AlixCell Death & Differentiation, 2004
- Programmed cell deathsEuropean Journal of Biochemistry, 2004
- The victorin‐induced mitochondrial permeability transition precedes cell shrinkage and biochemical markers of cell death, and shrinkage occurs without loss of membrane integrityThe Plant Journal, 2004
- Cell DeathCell, 2004
- A metacaspase of Trypanosoma brucei causes loss of respiration competence and clonal death in the yeast Saccharomyces cerevisiaeFEBS Letters, 2002
- Apoptotic mimicry by an obligate intracellular parasite downregulates macrophage microbicidal activityCurrent Biology, 2001
- Programmed cell death in trypanosomatidsParasitology Today, 1997