Document Type
Article
Publication Date
1-1-2016
Description
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.
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.
Citation Information
Chen, W.; Huang, Z.; Jiang, X.; Li, C.; and Gao, X.. 2016. Overexpression of Myeloid Differentiation Protein 88 in Mice Induces Mild Cardiac Dysfunction, but No Deficit in Heart Morphology. Brazilian Journal of Medical and Biological Research. Vol.49(1). https://doi.org/10.1590/1414-431X20154794 PMID: 26628395 ISSN: 0100-879X
Copyright Statement
This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.