Lan Yi and Eric T. Domyan contributed equally to this work.
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Fibroblast growth factor 9 signaling inhibits airway smooth muscle differentiation in mouse lung
Article first published online: 18 DEC 2008
DOI: 10.1002/dvdy.21831
Copyright © 2008 Wiley-Liss, Inc.
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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
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Lan Yi and Eric T. Domyan contributed equally to this work.
Publication History
- Issue published online: 18 DEC 2008
- Article first published online: 18 DEC 2008
- 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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Additional Supporting Information may be found in the online version of this article.
| Filename | Format | Size | Description |
|---|---|---|---|
| DVDY21831SuppFigS1.tif | 860K | Supp. Fig. S1. <I>Fgfr1;2-DKO</I> lungs are insensitive to the mesenchymal growth-promoting activity of FGF9. <B>A–H:</B> E11.5 lungs were cultured for 48 hr with or without FGF9 as indicated. Boxes in A, C, E, and G indicate regions that are magnified in B, D, F, and H, respectively. In the magnified views, the epithelial boundary (dashed lines) and the mesenchymal boundary (solid lines) are traced. The space between these lines indicates mesenchymal thickness. FGF9 added to the medium leads to an increase in mesenchyme thickness in normal control lungs (compare B and D), but not in <I>Fgfr1;2-DKO</I> lungs (compare F and H), suggesting that inactivation of <I>Fgfr1;2</I> largely blocks the ability of the mesenchyme to grow in response to FGF9. | |
| DVDY21831SuppFigS2.tif | 418K | Supp. Fig. S2. <I>Prdm6</I> is ectopically expressed in <I>Fgfr1;2-DKO</I> lungs. <B>A–D:</B> <I>Prdm6</I> expression as detected by RNA in situ hybridization. Boxed regions in A and C are magnified in B and D, respectively. Arrowheads in D indicate ectopic expression in distal mesenchyme. | |
| DVDY21831SuppFigS3.tif | 389K | Supp. Fig. S3. P-D markers are expressed in normal patterns in <I>Fgfr1;2-DKO</I> lungs. <B>A–F:</B> By RNA in situ hybridization, <I>Etv5</I> and <I>Nkx2.1</I> are both expressed in a normal pattern in the distal epithelium, and <I>Col2a1</I> also in a normal pattern in the proximal mesenchyme of <I>Fgfr1;2-DKO</I> lungs. | |
| DVDY21831SuppFigS4.tif | 398K | Supp. Fig. S4. Determining the dose of cyclopamine that inhibits SHH signaling in lung culture. <B>A, B:</B> Wild-type E11.5 lungs cultured in the presence of cyclopamine (cycl) at the indicated concentration. SHH signaling activity is indicated by <I>Ptch1</I> expression as assayed by RNA in situ hybridization. Lungs treated with 100 nM cycl show persistent signaling while lungs treated with 1 μM cycl show drastically reduced signaling. Cell death is observed in lungs cultured without cycl, possibility due to explanting of tissue. No obvious increase in cell death is observed in lungs treated with 1 μM cycl (data not shown). |
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