Lan Yi and Eric T. Domyan contributed equally to this work.
Fibroblast growth factor 9 signaling inhibits airway smooth muscle differentiation in mouse lung
Article first published online: 18 DEC 2008
Copyright © 2008 Wiley-Liss, Inc.
Volume 238, Issue 1, pages 123–137, January 2009
How to Cite
Yi, L., Domyan, E. T., Lewandoski, M. and Sun, X. (2009), Fibroblast growth factor 9 signaling inhibits airway smooth muscle differentiation in mouse lung. Dev. Dyn., 238: 123–137. doi: 10.1002/dvdy.21831
- Issue published online: 18 DEC 2008
- Article first published online: 18 DEC 2008
- Manuscript Accepted: 13 NOV 2008
- Burroughs-Wellcome. Grant Number: 1002361
- American Heart Association. Grant Number: 0610087Z
- NIH. Grant Number: 5T32GM07133
- fibroblast growth factor 9 (Fgf9);
- airway smooth muscle cells
In mammalian lungs, airway smooth muscle cells (airway SMCs) are present in the proximal lung adjacent to bronchi and bronchioles, but are absent in the distal lung adjacent to terminal sacs that expand during gas exchange. Evidence suggests that this distribution is essential for the formation of a functional respiratory tree, but the underlying genetic mechanism has not been elucidated. In this study, we test the hypothesis that fibroblast growth factor 9 (Fgf9) signaling is essential to restrict SMC differentiation to the proximal lung. We show that loss of Fgf9 or conditional inactivation of Fgf receptors (Fgfr) 1 and 2 in mouse lung mesenchyme results in ectopic SMCs. Our data support a model where FGF9 maintains a SMC progenitor population by suppressing differentiation and promoting growth. This model also represents our findings on the genetic relationship between FGF9 and sonic hedgehog (SHH) in the establishment of airway SMC pattern. Developmental Dynamics 238:123–137, 2009. © 2008 Wiley-Liss, Inc.