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. 2016 Aug 1;3:28. doi: 10.1186/s40348-016-0054-6

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© The Author(s). 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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Fig. 1 — Retinoid regulation of early lung development. a At the onset of lung development, mesodermal RA signaling suppresses Dkk1 to allow induction of Wnt pathway and inhibits Tgf-beta signaling to de-repress Fgf10 expression. Thus, RA coordinately controls proper Fgf10 levels to activate Fgf signaling to the foregut endoderm and form the lung primordium. RA regulation of Tgf-beta effects in endoderm has also been suggested. b During airway formation, mesodermal (mesenchymal) RA signaling restricts SM gene expression (Acta2, Myh11, Tagln) in distal lung, preventing ectopic and excessive SM differentiation while airways are branching. RA may potentially inhibit a key activator of SM transcription or induce a transcriptional repressor to control SM gene expression (diagram: myocardin, serum response factor, CArG DNA binding sites at SM gene promoters). Modified from Chen et al. [14, 15]