Journal
APOPTOSIS
Volume 18, Issue 6, Pages 653-663Publisher
SPRINGER
DOI: 10.1007/s10495-013-0822-x
Keywords
Trypanosoma cruzi; Trypomastigote; Amastigote; Cardiomyocyte; STAT3; Glycosylphosphatidylinositol
Categories
Funding
- Deutsche Stiftung fur Herzforschung
- Alumni Medizin Marburg e.V.
- Roland und Elfriede Schauer-Stiftung
- Studienstiftung des Deutschen Volkes
- BMBF [BRA 07/046]
- NIH [1RO1AI071319-01]
- INCTV/CNPq [573547/2008-4]
- FAPEMIG [CBB-APQ-01603-09, CBB-APQ-00077-09]
- program PROBRAL of DAAD/CAPES
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI071319] Funding Source: NIH RePORTER
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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.
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