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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Early dystrophin disruption in the pathogenesis of experimental chronic Chagas cardiomyopathy

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Author(s):
Prado, Cibele M. [1] ; Celes, Mara R. N. ; Malvestio, Lygia M. ; Campos, Erica C. ; Silva, Joao S. [2] ; Jelicks, Linda A. [3] ; Tanowitz, Herbert B. [1] ; Rossi, Marcos A. [4]
Total Authors: 8
Affiliation:
[1] Albert Einstein Coll Med, Dept Pathol, Bronx, NY 10467 - USA
[2] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Biochem & Immunol, BR-14049900 Ribeirao Preto, SP - Brazil
[3] Albert Einstein Coll Med, Dept Physiol & Biophys, Bronx, NY 10467 - USA
[4] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Pathol, Lab Cellular & Mol Cardiol, BR-14049900 Ribeirao Preto, SP - Brazil
Total Affiliations: 4
Document type: Journal article
Source: Microbes and Infection; v. 14, n. 1, p. 59-68, JAN 2012.
Web of Science Citations: 7
Abstract

Chronic Chagas cardiomyopathy evolves over a long period of time after initial infection by Trypanosoma cruzi. Similarly, a cardiomyopathy appears later in life in muscular dystrophies. This study tested the hypothesis that dystrophin levels are decreased in the early stage of T cruzi-infected mice that precedes the later development of a cardiomyopathy. CD1 mice were infected with T cruzi (Brazil strain), killed at 30 and 100 days post infection (dpi), and the intensity of inflammation, percentage of interstitial fibrosis, and dystrophin levels evaluated. Echocardiography and magnetic resonance imaging data were evaluated from 15 to 100 dpi. At 30 dpi an intense acute myocarditis with ruptured or intact intracellular parasite nests was observed. At 100 dpi a mild chronic fibrosing myocarditis was detected without parasites in the myocardium. Dystrophin was focally reduced or completely lost in cardiomyocytes at 30 dpi, with the reduction maintained up to 100 dpi. Concurrently, ejection fraction was reduced and the right ventricle was dilated. These findings support the hypothesis that the initial parasitic infection-induced myocardial dystrophin reduction/loss, maintained over time, might be essential to the late development of a cardiomyopathy in mice. (C) 2011 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved. (AU)

FAPESP's process: 10/13199-1 - Dystrophin and its associated proteins in the pathogenesis of doxorubicin-induced cardiomyopathy
Grantee:Marcos Antonio Rossi
Support Opportunities: Regular Research Grants
FAPESP's process: 09/17787-8 - High blood pressure, cardiac hypertrophy, heart failure and dystrophin-glycoprotein complex
Grantee:Cibele Maria Prado Zinni
Support Opportunities: Research Grants - Young Investigators Grants
FAPESP's process: 10/19216-5 - Hypertension, cardiac hypertrophy and cardiac failure and dystrophin glycoproteins
Grantee:Cibele Maria Prado Zinni
Support Opportunities: Scholarships in Brazil - Young Researchers
FAPESP's process: 10/18629-4 - The role of calcium, calpain, pro-inflammatory cytokines and hypoxia on dystrophin expression in cardiomyocytes subjected to different stimuli: an in vitro study
Grantee:Lygia Maria Mouri Malvestio
Support Opportunities: Scholarships in Brazil - Doctorate (Direct)
FAPESP's process: 09/54010-1 - Sepsis and septic shock: functional and morphological changes in the heart. An experimental study in mice
Grantee:Helio Cesar Salgado
Support Opportunities: Multi-user Equipment Program