Author | Durand, Jorge L. | |
Author | Mukherjee, Shankar | |
Author | Commodari, Fernando | |
Author | Souza, Andrea P. de | |
Author | Zhao, Dazhi | |
Author | Machado, Fabiana S. | |
Author | Tanowitz, Herbert B. | |
Author | Jelicks, Linda A. | |
Access date | 2018-09-21T23:43:39Z | |
Available date | 2018-09-21T23:43:39Z | |
Document date | 2009 | |
Citation | DURAND, Jorge L. et al. Role of NO Synthase in the Development of Trypanosoma cruzi– Induced Cardiomyopathy in Mice. Am J Trop Med Hyg., v.80, n.5, p,782-787, May 2009. | pt_BR |
ISSN | 0002-9637 | pt_BR |
URI | https://www.arca.fiocruz.br/handle/icict/28981 | |
Language | eng | pt_BR |
Publisher | The American Society of Tropical Medicine and Hygiene | pt_BR |
Rights | restricted access | |
Subject in Portuguese | Trypanosoma cruzi | pt_BR |
Subject in Portuguese | Cardiomiopatia | pt_BR |
Subject in Portuguese | Inflamação | pt_BR |
Subject in Portuguese | Camundongos | pt_BR |
Subject in Portuguese | Óxido Nítrico Sintase | pt_BR |
Title | Role of NO Synthase in the Development of Trypanosoma cruzi– Induced Cardiomyopathy in Mice | pt_BR |
Type | Article | |
Abstract | 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. | pt_BR |
Affilliation | Albert Einstein College of Medicine. Department of Physiology and Biophysics. Bronx, NY . USA. | pt_BR |
Affilliation | Albert Einstein College of Medicine. Department of Pathology. Bronx, NY, USA. | pt_BR |
Affilliation | R&D Department. Franklin Lakes, NJ, USA. | pt_BR |
Affilliation | Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil. | pt_BR |
Affilliation | Albert Einstein College of Medicine. Department of Pathology. Bronx, NY, USA. | pt_BR |
Affilliation | Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Belo Horizonte, MG, Brasil. | pt_BR |
Affilliation | Albert Einstein College of Medicine. Department of Pathology and Medicine. Bronz. NY, USA. | pt_BR |
Affilliation | Albert Einstein College of Medicine. Department of Physiology and Biophysics. Bronx, MY, USA. | pt_BR |
Subject | Trypanosoma cruzi | pt_BR |
Subject | Cardiomyopathy | pt_BR |
Subject | inflammation | pt_BR |
Subject | Mice | pt_BR |
Subject | NO synthase | pt_BR |
e-ISSN | 1476-1645 | |
Embargo date | 2030-01-01 | |