Inhibitory Smad proteins promote the differentiation of mouse embryonic stem cells into ependymal-like ciliated cells.
Motile cilia play crucial roles in the maintenance of homeostasis in vivo. Defects in the biosynthesis of cilia cause immotile cilia syndrome, also known as primary ciliary dyskinesia (PCD), which is associated with a variety of complex diseases. In this study, we found that inhibitory Smad proteins, Smad7 and Smad6, significantly promoted the differentiation of mouse embryonic stem (ES) cells into ciliated cells. Moreover, these Smad proteins specifically induced morphologically distinct Musashi1-positive ciliated cells. These results suggest that inhibitory Smad proteins could be important regulators not only for the regulation of ciliated cell differentiation, but also for the subtype specification of ciliated cells during differentiation from mouse ES cells.
Nishimura
Yusuke
Y
Department of Biological Science, Graduate School of Science, The University of Tokyo, 3-8-1 Komaba, Meguro-ku, Tokyo 153-8902, Japan.
Kurisaki
Akira
A
Nakanishi
Mio
M
Ohnuma
Kiyoshi
K
Ninomiya
Naoto
N
Komazaki
Shinji
S
Ishiura
Shoichi
S
Asashima
Makoto
M
D000818:Animals; D002454:Cell Differentiation; D002460:Cell Line; D002923:Cilia / Q000502:physiology; D053595:Embryonic Stem Cells / Q000502:physiology*; D004805:Ependyma / Q000166:cytology* / Q000502:physiology; D051379:Mice; D051905:Smad6 Protein / Q000235:genetics / Q000502:physiology*; D051906:Smad7 Protein / Q000235:genetics / Q000502:physiology*
D051905:Smad6 Protein; C497803:Smad6 protein, mouse; D051906:Smad7 Protein; C497807:Smad7 protein, mouse