Overexpression of myeloid differentiation protein 88 in mice induces mild cardiac dysfunction, but no deficit in heart morphology
Braz. j. med. biol. res
;
49(1): e4794, 2016. graf
Artículo
en Inglés
| LILACS
| ID: biblio-951643
ABSTRACT
Cardiac remodeling involves changes in heart shape, size, structure, and function after injury to the myocardium. The proinflammatory adaptor protein myeloid differentiation protein 88 (MyD88) contributes to cardiac remodeling. To investigate whether excessive MyD88 levels initiate spontaneous cardiac remodeling at the whole-organism level, we generated a transgenic MyD88 mouse model with a cardiac-specific promoter. MyD88 mice (male, 20-30 g, n=∼80) were born at the expected Mendelian ratio and demonstrated similar morphology of the heart and cardiomyocytes with that of wild-type controls. Although heart weight was unaffected, cardiac contractility of MyD88 hearts was mildly reduced, as shown by echocardiographic examination, compared with wild-type controls. Moreover, the cardiac dysfunction phenotype was associated with elevation of ANF and BNP expression. Collectively, our data provide novel evidence of the critical role of balanced MyD88 signaling in maintaining physiological function in the adult heart.
Texto completo:
Disponible
Índice:
LILACS (Américas)
Asunto principal:
Remodelación Ventricular
/
Factor 88 de Diferenciación Mieloide
/
Cardiopatías
Tipo de estudio:
Estudio pronóstico
Límite:
Animales
Idioma:
Inglés
Revista:
Braz. j. med. biol. res
Asunto de la revista:
Biologia
/
Medicina
Año:
2016
Tipo del documento:
Artículo
País de afiliación:
China
/
Estados Unidos
Institución/País de afiliación:
East Tennessee State University/US
/
Nanjing University/CN
/
Soochow University/CN
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