FGF-16 is required for embryonic heart development

Fibroblast growth factor 16 (FGF-16) expression has previously been detected in mouse heart at mid-gestation in the endocardium and epicardium, suggesting a role in embryonic heart development. More specifically, exogenously applied FGF-16 has been shown to stimulate growth of embryonic myocardial c...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2008-08, Vol.373 (2), p.270-274
Main Authors: Lu, Shun Yan, Sheikh, Farah, Sheppard, Patricia C., Fresnoza, Agnes, Duckworth, Mary Lynn, Detillieux, Karen A., Cattini, Peter A.
Format: Article
Language:English
Subjects:
Animals
Craniofacial Abnormalities - genetics
Embryo Loss - genetics
Female
Fibroblast growth factor
Fibroblast Growth Factors - genetics
Gene Targeting
Heart
Heart - embryology
Heart Defects, Congenital - genetics
Heart Defects, Congenital - pathology
Mice
Mice, Knockout
Mid-gestation
Mouse
Myocardial defect
Pregnancy
Pregnancy Trimester, Second
X Chromosome - genetics
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Summary:Fibroblast growth factor 16 (FGF-16) expression has previously been detected in mouse heart at mid-gestation in the endocardium and epicardium, suggesting a role in embryonic heart development. More specifically, exogenously applied FGF-16 has been shown to stimulate growth of embryonic myocardial cells in tissue explants. We have generated mice lacking FGF-16 by targeting the Fgf16 locus on the X chromosome. Elimination of Fgf16 expression resulted in embryonic death as early as day 11.5 (E11.5). External abnormalities, including hemorrhage in the heart and ventral body region as well as facial defects, began to appear in null embryos from E11.5. Morphological analysis of FGF-16 null hearts revealed cardiac defects including chamber dilation, thinning of the atrial and ventricular walls, and poor trabeculation, which were visible at E10.5 and more pronounced at E11.5. These findings indicate FGF-16 is required for embryonic heart development in mid-gestation through its positive effect on myocardial growth.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2008.06.029