TY - JOUR
T1 - Gene expression changes associated with myocarditis and fibrosis in hearts of mice with chronic chagasic cardiomyopathy
AU - Soares, Milena Botelho Pereira
AU - De Lima, Ricardo Santana
AU - Rocha, Leonardo Lima
AU - Vasconcelos, Juliana Fraga
AU - Rogatto, Silvia Regina
AU - Dos Santos, Ricardo Ribeiro
AU - Iacobas, Sanda
AU - Goldenberg, Regina Coeli
AU - Iacobas, Dumitru Andrei
AU - Tanowitz, Herbert Bernard
AU - De Carvalho, Antonio Carlos Campos
AU - Spray, David Conover
N1 - Funding Information:
Financial support: National Institutes of Health (grants HL-73732, HD-32573, AI-076248, and AI-052739), Coordenac¸ão de Aperfeic¸oamento de Pessoal de Nível Superior, Conselho Nacional de Desenvolvimento Científico e Tecnológico, Fundac¸ão de Amparo à Pesquisa do Estado do Rio de Janeiro, Fundac¸ão de Amparo à Pesquisa do Estado da Bahia, and Fogarty International Center (training grant D43TW007129 to R.C.G. and L.L.R.).
PY - 2010/8/1
Y1 - 2010/8/1
N2 - Chronic chagasic cardiomyopathy is a leading cause of heart failure in Latin American countries. About 30% of Trypanosoma cruzi-infected individuals develop this severe symptomatic form of the disease, characterized by intense inflammatory response accompanied by fibrosis in the heart.We performed an extensive microarray analysis of hearts from a mouse model of this disease and identified significant alterations in expression of ~12% of the sampled genes. Extensive up-regulations were associated with immune-inflammatory responses (chemokines, adhesion molecules, cathepsins, and major histocompatibility complex molecules) and fibrosis (extracellular matrix components, lysyl oxidase, and tissue inhibitor of metalloproteinase 1). Our results indicate potentially relevant factors involved in the pathogenesis of the disease that may provide newtherapeutic targets in chronic Chagas disease.
AB - Chronic chagasic cardiomyopathy is a leading cause of heart failure in Latin American countries. About 30% of Trypanosoma cruzi-infected individuals develop this severe symptomatic form of the disease, characterized by intense inflammatory response accompanied by fibrosis in the heart.We performed an extensive microarray analysis of hearts from a mouse model of this disease and identified significant alterations in expression of ~12% of the sampled genes. Extensive up-regulations were associated with immune-inflammatory responses (chemokines, adhesion molecules, cathepsins, and major histocompatibility complex molecules) and fibrosis (extracellular matrix components, lysyl oxidase, and tissue inhibitor of metalloproteinase 1). Our results indicate potentially relevant factors involved in the pathogenesis of the disease that may provide newtherapeutic targets in chronic Chagas disease.
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U2 - 10.1086/653481
DO - 10.1086/653481
M3 - Article
C2 - 20565256
AN - SCOPUS:77954738641
SN - 0022-1899
VL - 202
SP - 416
EP - 426
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
IS - 3
ER -
