Overexpression of myeloid differentiation protein 88 in mice induces mild cardiac dysfunction, but no deficit in heart morphology
Rev. bras. pesqui. méd. biol
; Braz. j. med. biol. res;49(1): e4794, 2016. graf
Article
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| LILACS
| ID: biblio-951643
Bibliothèque responsable:
BR1.1
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.
Mots clés
Texte intégral:
1
Indice:
LILACS
Sujet Principal:
Remodelage ventriculaire
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Facteur de différenciation myéloïde-88
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Cardiopathies
Type d'étude:
Prognostic_studies
Limites du sujet:
Animals
langue:
En
Texte intégral:
Braz. j. med. biol. res
/
Rev. bras. pesqui. méd. biol
Thème du journal:
BIOLOGIA
/
MEDICINA
Année:
2016
Type:
Article