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ArtículoDerechos de autor
Acceso restringido
Fecha del embargo
2030-01-01
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- IOC - Artigos de Periódicos [12500]
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ROLE OF NO SYNTHASE IN THE DEVELOPMENT OF TRYPANOSOMA CRUZI– INDUCED CARDIOMYOPATHY IN MICE
Cardiomiopatia
Inflamação
Camundongos
Óxido Nítrico Sintase
Autor
Afiliación
Albert Einstein College of Medicine. Department of Physiology and Biophysics. Bronx, NY . USA.
Albert Einstein College of Medicine. Department of Pathology. Bronx, NY, USA.
R&D Department. Franklin Lakes, NJ, USA.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil.
Albert Einstein College of Medicine. Department of Pathology. Bronx, NY, USA.
Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Belo Horizonte, MG, Brasil.
Albert Einstein College of Medicine. Department of Pathology and Medicine. Bronz. NY, USA.
Albert Einstein College of Medicine. Department of Physiology and Biophysics. Bronx, MY, USA.
Albert Einstein College of Medicine. Department of Pathology. Bronx, NY, USA.
R&D Department. Franklin Lakes, NJ, USA.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil.
Albert Einstein College of Medicine. Department of Pathology. Bronx, NY, USA.
Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Belo Horizonte, MG, Brasil.
Albert Einstein College of Medicine. Department of Pathology and Medicine. Bronz. NY, USA.
Albert Einstein College of Medicine. Department of Physiology and Biophysics. Bronx, MY, USA.
Resumen en ingles
Trypanosoma cruzi infection results in an increase in myocardial NO and intense inflammation. NO modulates the T. cruzi–induced myocardial inflammatory reaction. NO synthase (NOS)1-, NOS2-, and NOS3-null mice were infected with T. cruzi (Brazil strain). Infected NOS1-null mice had increased parasitemia, mortality, and left ventricular inner diameter (LVID). Chronically infected NOS1- and NOS2-null and wild-type mice (WT) exhibited increased right ventricular internal diameter (RVID), although the fold increase in the NOS2-null mice was smaller. Infected NOS3null mice exhibited a significant reduction both in LVID and RVID. Reverse transcriptasepolymerase chain reaction showed expression of NOS2 and NOS3 in hearts of infected NOS1-null and WT mice, whereas infected NOS2-null hearts showed little change in expression of other NOS isoforms. Infected NOS3-null hearts showed an increase only in NOS1 expression. These results may indicate different roles for NOS isoforms in T. cruzi–induced cardiomyopathy.
Palabras clave en portugues
Trypanosoma cruziCardiomiopatia
Inflamação
Camundongos
Óxido Nítrico Sintase
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