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Possible role of dystrophin and integrin-associated glycoprotein complex in sudden death in experimental Chagas disease

Grant number: 08/00954-6
Support type:Scholarships abroad - Research
Effective date (Start): July 14, 2008
Effective date (End): December 13, 2008
Field of knowledge:Health Sciences - Medicine - Pathological Anatomy and Clinical Pathology
Principal researcher:Cibele Maria Prado Zinni
Grantee:Cibele Maria Prado Zinni
Host: Herbert Bernard Tanowitz
Home Institution: Pessoa Física
Research place: Albert Einstein College of Medicine, United States  

Abstract

Chagas' disease, caused by the protozoan flagellate Trypanosoma cruzi infection, is endemic in 21 countries of South and Central Americas. The transmission via insects has been efficiently controlled in affected areas and blood transfusion and congenital infection are the most important sources of the disease in humans. Experimental production of Chagas' disease through infection of mice with T.cruzi has been used to study the pathophysiological mechanisms of the disease and host protection. Studies in collaboration with other laboratories have demonstrated that after the parasitemia peak, the parasitemia decreases and the animals begin to die suddenly 25-30 after infection. Heart failure, in addition to functional alterations, has a structural basis as well. This concerns all components of the cardiac myocytes as well as the extracellular space. In addition to proteins of cardiomyocytes, like contractile proteins, sarcomeric proteins, cytoskeleton proteins, there are a group of proteins that contribute to the interaction of intracellular cytoskeleton to the extracellular matrix. These proteins include dystrophin, dystrophin glycoprotein complex and vinculin-integrin interaction. The objectives of the present study are evaluate the organization, the expression of dystrophin glycoprotein complex proteins and its relation with proteins of the cytoskeleton in the subacute phase of the experimental infection by T. cruzi, that is, elucidate the role of cytoskeleton proteins and proteins that contribute to the interaction of intracellular cytoskeleton to the extracellular matrix, to find a plausible explanation to sudden death during the evolution of the disease. Moreover, additional data from morphological studies and cardiac function, including echocardiogram and magnetic resonance, could help the understanding of the cardiac alterations observed previously the death of the animals. (AU)

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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
ROSSI‚ M.A.; TANOWITZ‚ H.B.; MALVESTIO‚ L.M.; CELES‚ M.R.; CAMPOS‚ E.C.; BLEFARI‚ V.; PRADO‚ C.M.. Coronary microvascular disease in chronic Chagas cardiomyopathy including an overview on history‚ pathology‚ and other proposed pathogenic mechanisms. PLoS Neglected Tropical Diseases, v. 4, n. 8, p. e674, . (08/00954-6)
ROSSI, MARCOS A.; TANOWITZ, HERBERT B.; MALVESTIO, LYGIA M.; CELES, MARA R.; CAMPOS, ERICA C.; BLEFARI, VALDECIR; PRADO, CIBELE M.. Coronary Microvascular Disease in Chronic Chagas Cardiomyopathy Including an Overview on History, Pathology, and Other Proposed Pathogenic Mechanisms. PLoS Neglected Tropical Diseases, v. 4, n. 8, . (08/00954-6)
PRADO, CIBELE M.; FINE, EUGENE J.; KOBA, WADE; ZHAO, DAZHI; ROSSI, MARCOS A.; TANOWITZ, HERBERT B.; JELICKS, LINDA A.. Micro-Positron Emission Tomography in the Evaluation of Trypanosoma cruzi-Induced Heart Disease: Comparison with Other Modalities. American Journal of Tropical Medicine and Hygiene, v. 81, n. 5, p. 900-905, . (08/00954-6)

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