First published online April 22, 2004
Development 131, 905e (2004)
© The Company of Biologists Limited
BMP10 – a heartfelt balance
During mid-gestation in the mouse, cardiogenesis switches from patterning
processes to growth and chamber formation. Disruption of this transition can
lead to a variety of congenital heart diseases, and, on
p. 2219, Chen et al.
shed some light on the mechanisms underlying these defects. During the
mid-gestation transition, the trabecular myocardium proliferates to generate
myocytes that contribute the future ventricular septum, papillary muscles and
conduction system. It has been shown previously that mice lacking
FK506-binding protein 12 die because of an overproduction of ventricular
trabeculae, and that BMP10, which is normally transiently expressed in the
trabecular myocardium, is upregulated in these hypertrabeculated hearts. Chen
and colleagues have found that in the myocardium of mice lacking BMP10, the
negative cell-cycle regulator p57kip2 is upregulated and that
cardiomyocyte proliferation is reduced. Furthermore, cardiogenic factors (e.g.
NKX2.5 and MEF2C) are downregulated. They conclude that BMP10 is a positive
cardiomyocyte growth signal that, together with negative cell-cycle
regulators, orchestrates the balance between proliferation and terminal
differentiation.
Related articles in Development:
- BMP10 is essential for maintaining cardiac growth during murine cardiogenesis
- Hanying Chen, Shu Shi, Lourdes Acosta, Weiming Li, Jonathan Lu, Shideng Bao, Zhuang Chen, Zuocheng Yang, Michael D. Schneider, Kenneth R. Chien, Simon J. Conway, Mervin C. Yoder, Laura S. Haneline, Diego Franco, and Weinian Shou
Development 2004 131: 2219-2231.
[Abstract]
[Full Text]
