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Beta-catenin activation and upregulation of BMP4 expression. A-B: IHC using an antibody that is specific for activated beta-catenin dephosphorylated on Ser37 or Thr4, and an antibody that recognizes only membrane bound beta-catenin. Counterstained with Hoechst (hst). A: Wildtype alveolar lung contains scattered cells with activated beta-catenin. B: Beta-catenin is activated in more cells in the transgenic lung. A': magnification from A. B' Magnification from B. In both WT and TG, cells are double positive for activated and membrane-bound beta-catenin, implying that cells retain membrane-bound beta-catenin even when activated. C-D: ISH using a probe for Bmp4. Bmp4 was expressed in both wildtype (C) and transgenic (D) distal lung epithelium, but transgenic expression was much more widespread. Part of the right atrium (Bmp4 negative) is seen to the right hand side of the TG lung lobe in D. E: Multiplex-RTPCR of E14.5 wildtype and transgenic lung using primers for G6pd-2 (Glucose-6-phosphate dehydrogenase gene), Bmp4 and Bmp5 shows upregulation of Bmp4 mRNA.
Cells positive for activated beta-catenin were present throughout
the epithelium and mesenchyme in both wildtype and transgenic lobes
(Fig 8A–B), and more activated cells were present in the distal
part of the wildtype lung (data not shown), than the proximal part
The frequency of activated beta-catenin cells was higher in the
transgenic lobes, especially in the proximal lung (Fig 8B) but also
in the distal lung (data not shown), suggesting that Fgf10
overexpression leads to activation of beta-catenin. .
In situ hybridization revealed that Bmp4 was expressed in scattered
epithelial cells at E18.5 (Fig 8C), while the number of Bmp4
positive cells was increased in transgenic lungs (Fig 8D).
This result was confirmed by MPX RT-PCR, where Bmp4 but not Bmp5
expression was highly upregulated in transgenic lungs (Fig 8E)..
Nyeng, Pia; Norgaard, Gitte A; Kobberup, Sune; Jensen, JanJournal: BMC Developmental Biology
Issue 1DOI: 10.1186/1471-213X-8-2Published: 2008-12-01Institution(s):
Lerner Research Institute, Stem Cell Biology and Regenerative Medicine, Barbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center
This image is from the article titled "FGF10 maintains distal lung bud epithelium and excessive signaling leads to progenitor state arrest, distalization, and goblet cell metaplasia"
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