Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/30195
Title: Trypomastigotes and amastigotes of Trypanosoma cruzi induce apoptosis and STAT3 activation in cardiomyocytes in vitro.
Authors: Stahl, Philipp
Ruppert, Volker
Meyer, Thomas
Schmidt, Jorg
Campos, Marco Antonio
Gazzinelli, Ricardo Tostes
Maisch, Bernhard
Schwarz, Ralph T.
Debierre-Grockiego, Francoise
Affilliation: Laboratory of Parasitology. Institute for Virology. Philipps University. Marburg, Germany
Department of Cardiology, Philipps University, Marburg, Germany/Department of Cardiology, Philipps University, Marburg, Germany
Department of Psychosomatic Medicine and Psychotherapy, Georg August University, 37075 Gottingen, Germany/ Department of Cardiology, Philipps University, Marburg, Germany
Laboratory of Parasitology. Institute for Virology. Philipps University. Marburg, Germany
Fundação Oswaldo Cruz. Centro de Pesquisa Rene Rachou. Belo Horizonte, MG, Brazil
Fundação Oswaldo Cruz. Centro de Pesquisa Rene Rachou. Belo Horizonte, MG, Brazil/Division of Infectious Diseases and Immunology. Department of Medicine. University of Massachusetts Medical School, Worcester, MA, USA/Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Belo Horizonte, MG, Brazil
Department of Cardiology, Philipps University, Marburg, Germany
CNRS-UMR 8576, Unit of Structural and Functional Glycobiology. Univ Lille Nord de France, Lille, France/ Laboratory of Parasitology. Institute for Virology. Philipps University. Marburg, Germany
Universite Francois Rabelais de Tours. UMR 1282 Infectiologie et Sante Publique. Tours, France/INRA, UMR 1282 Infectiologie et Sante Publique. Nouzilly, France/Laboratory of Parasitology. Institute for Virology. Philipps University. Marburg, Germany
Abstract: The haemoflagellate Trypanosoma cruzi is the causative agent of Chagas' disease that occurs in approximately 8 million people in Latin America. Patients infected with T. cruzi frequently suffer of cardiomegaly and may die of myocardial failure. Here we show that T. cruzi trypomastigotes (extracellular form) increased in vitro apoptosis of rat cardiomyocytes. Additionally, we demonstrated that amastigotes (intracellular form), for which a method for purification was established, were also able to induce cardiomyocyte apoptosis. Increase of apoptosis was associated with up-regulation of the apoptotic gene bax by trypomastigotes, while expression of the anti-apoptotic gene bcl-2 was down-regulated by amastigotes. The transcription factor STAT3 but not STAT1 was activated in cardiomyocytes by trypomastigotes. In addition, tlr7 gene expression was up-regulated in cardiomyocytes incubated with trypomastigotes, suggesting that this Toll-like receptor is involved in the intracellular recognition after host cell invasion by T. cruzi. Glycosylphosphatidylinositols purified from trypomastigotes did not induce cardiomyocyte apoptosis and STAT activation but down-regulated tlr7 gene expression. In conclusion, cardiomyopathy observed in Chagas' disease might be in part due to apoptosis of cardiomyocytes induced directly by the parasite.
Keywords: Trypanosoma cruzi
Trypomastigote
Amastigote
Cardiomyocyte
STAT3 Glycosylphosphatidylinositol
keywords: Trypanosoma cruzi
tripomastigota
Amastigota
Cardiomiócito
Issue Date: 2013
Publisher: Springer
Citation: STAHL, Philipp et al. Trypomastigotes and amastigotes of Trypanosoma cruzi induce apoptosis and STAT3 activation in cardiomyocytes in vitro. Apoptosis., v. 18, n. 6, p. 653-63, 2013
DOI: 10.1007/s10495-013-0822-x
ISSN: 1360-8185
Copyright: restricted access
Appears in Collections:MG - IRR - Artigos de Periódicos

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