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
Article
in English
| 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.
Full text:
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Index:
LILACS (Americas)
Main subject:
Ventricular Remodeling
/
Myeloid Differentiation Factor 88
/
Heart Diseases
Type of study:
Prognostic study
Limits:
Animals
Language:
English
Journal:
Braz. j. med. biol. res
Journal subject:
Biology
/
Medicine
Year:
2016
Type:
Article
Affiliation country:
China
/
United States
Institution/Affiliation country:
East Tennessee State University/US
/
Nanjing University/CN
/
Soochow University/CN
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