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. Author manuscript; available in PMC: 2017 Jun 15.
Published in final edited form as: Dev Biol. 2016 Apr 30;414(2):161–169. doi: 10.1016/j.ydbio.2016.04.023

Figure 5. Systemic activation of Wnt/β-catenin signaling alleviates the defects of lung sacculation and AT1 cell differentiation in the HDAC3Dermo1creKO lungs.

Figure 5

(A-F) H&E staining shows that the sacculation defects at E18.5 are improved in LiCl-treated HDAC3Dermo1creKO lungs compared to NaCl treated HDAC3Dermo1creKO lungs. (G) Quantification of distal airway area indicates that the sacculation defect is partially restored in LiCl-treated HDAC3Dermo1creKO lungs at E18.5. (H-K) Aqp5 immunostaining and Q-PCR show that the defect in AT1 cell differentiation is significantly rescued in LiCl-treated HDAC3Dermo1creKO lungs compared to NaCl-treated mutants at E18.5 (J, arrows). LiCl treatment also rescues expression of Axin2 and Lef-1 in HDAC3Dermo1creKO mutants.

Ctrl=Control; KO= HDAC3Dermo1creKO lungs. Two tail student's t test: **p<0.01. n=3. Q-PCR data are represented as mean ± SD. Scale Bars: E=50μm; F and J=100 μm.