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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.)

Role of dystrophin in acute Trypanosoma cruzi infection

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Author(s):
Malvestio, Lygia M. [1] ; Celes, Mara R. N. [1, 2, 3] ; Milanezi, Cristiane [4] ; Silva, Joao S. [4] ; Jelicks, Linda A. [5] ; Tanowitz, Herbert B. [3] ; Rossi, Marcos A. [1] ; Prado, Cibele M. [1, 3]
Total Authors: 8
Affiliation:
[1] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Pathol, BR-14049900 Ribeirao Preto, SP - Brazil
[2] Univ Fed Goias, Inst Trop Pathol & Publ Hlth, Goiania, Go - Brazil
[3] Albert Einstein Coll Med, Dept Pathol, Bronx, NY 10467 - USA
[4] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Biochem & Immunol, BR-14049900 Ribeirao Preto, SP - Brazil
[5] Albert Einstein Coll Med, Dept Physiol & Biophys, Bronx, NY 10467 - USA
Total Affiliations: 5
Document type: Journal article
Source: Microbes and Infection; v. 16, n. 9, p. 768-777, SEP 2014.
Web of Science Citations: 3
Abstract

Previous studies have demonstrated loss/reduction of dystrophin in cardiomyocytes in both acute and chronic stages of experimental Trypanosoma cruzi (T cruzi) infection in mice. The mechanisms responsible for dystrophin disruption in the hearts of mice acutely infected with T cruzi are not completely understood. The present in vivo and in vitro studies were undertaken to evaluate the role of inflammation in dystrophin disruption and its correlation with the high mortality rate during acute infection. C57BL/6 mice were infected with T cruzi and killed 14, 20 and 26 days post infection (dpi). The intensity of inflammation, cardiac expression of dystrophin, calpain-1, NF-kappa B, TNF-alpha, and sarcolemmal permeability were evaluated. Cultured neonatal marine cardiomyocytes were incubated with serum, collected at the peak of cytokine production and free of parasites, from T cruzi-infected mice and dystrophin, calpain-1, and NF-kappa B expression analyzed. Dystrophin disruption occurs at the peak of mortality and inflammation and is associated with increased expression of calpain-1, TNF-alpha, NF-kappa B, and increased sarcolemmal permeability in the heart of T cruzi-infected mice at 20 dpi confirmed by in vitro studies. The peak of mortality occurred only when significant loss of dystrophin in the hearts of infected animals occurred, highlighting the correlation between inflammation, dystrophin loss and mortality. (C) 2014 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved. (AU)

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)