Drs. Hotta and Sasaki contributed equally to this work.
Special Issue Research Article
Fgf16 is required for cardiomyocyte proliferation in the mouse embryonic heart†
Article first published online: 24 SEP 2008
Copyright © 2008 Wiley-Liss, Inc.
Special Issue: Special Focus on the Extracellular Matrix, in Memory of Dr. Elizabeth D. Hay
Volume 237, Issue 10, pages 2947–2954, October 2008
How to Cite
Hotta, Y., Sasaki, S., Konishi, M., Kinoshita, H., Kuwahara, K., Nakao, K. and Itoh, N. (2008), Fgf16 is required for cardiomyocyte proliferation in the mouse embryonic heart. Dev. Dyn., 237: 2947–2954. doi: 10.1002/dvdy.21726
This article was accepted for inclusion in the Special Focus on FGF/RTK Signalling, which will publish in December 2008.
- Issue published online: 24 SEP 2008
- Article first published online: 24 SEP 2008
- Manuscript Accepted: 4 AUG 2008
- Ministry of Education, Science, Culture, Sports, and Technology, Japan
- Takeda Science Foundation
- Mitsubishi Foundation
Fibroblast growth factor (Fgf) signaling plays important roles in development and metabolism. Mouse Fgf16 was predominantly expressed in cardiomyocytes. To elucidate the physiological roles of Fgf16, we generated Fgf16 knockout mice. Although the mice were apparently normal and fertile, heart weight and cardiomyocyte cell numbers were slightly decreased at 6 months of age. However, blood pressure, heart rate, and cardiac performance were essentially unchanged. In addition, the expression of most cardiac marker genes examined was also essentially unchanged. However, the expression of Bnp was significantly decreased, indicating potential roles of Fgf16 in the heart under pathological conditions. In contrast, the proliferation of embryonic cardiomyocytes was significantly decreased, indicating that Fgf16 is a growth factor for these cells. The embryonic heart phenotype is similar to that of the Fgf9 knockout heart, indicating Fgf9 and Fgf16 to synergistically act as growth factors for embryonic cardiomyocytes. Developmental Dynamics 237:2947–2954, 2008. © 2008 Wiley-Liss, Inc.