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Fibroblast growth factor 9 signaling inhibits airway smooth muscle differentiation in mouse lung

  1. Lan Yi1,†,
  2. Eric T. Domyan1,†,
  3. Mark Lewandoski2,
  4. Xin Sun1,*

Article first published online: 18 DEC 2008

DOI: 10.1002/dvdy.21831

Issue

Developmental Dynamics

Developmental Dynamics

Volume 238, Issue 1, pages 123–137, January 2009

Additional Information

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

Author Information

  1. 1

    Laboratory of Genetics, University of Wisconsin-Madison, Madison, Wisconsin

  2. 2

    Cancer and Developmental Biology Lab, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, Maryland

  1. †

    Lan Yi and Eric T. Domyan contributed equally to this work.

*Laboratory of Genetics, University of Wisconsin-Madison, Madison, WI 53706

  1. †

    Lan Yi and Eric T. Domyan contributed equally to this work.

Publication History

  1. Issue published online: 18 DEC 2008
  2. Article first published online: 18 DEC 2008
  3. Manuscript Accepted: 13 NOV 2008

Funded by

  • Burroughs-Wellcome. Grant Number: 1002361
  • American Heart Association. Grant Number: 0610087Z
  • NIH. Grant Number: 5T32GM07133

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Keywords:

  • fibroblast growth factor 9 (Fgf9);
  • lung;
  • airway smooth muscle cells

Abstract

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.

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