Inhibition of PKA signaling blocks microtia development in Bmpr1a-deficient mice
A. Diagram showing the schedule of TAM and H89 administration.
B. Immunostaining results of p-Creb in ear sections of the H89-treated mutant and control mice. Scale bars=50 μm.
C. The rescue of the microtia phenotype in the mutant mice by H89. Right panels: Quantitation data. N=3.
D. H/E staining results. Right panels: the thickness of the cartilage and the size of the chondrocytes in the ear of the mutant and control mice. N=3. Right panels: Quantitation data. Scale bars=50 μm. N=3.
E. Immunostaining results for Col1α1 in the ear sections of the H89-treated mutant and control mice. Scale bars=20 μm. Arrows: positive signals.
F. ALP activity was greatly suppressed by H89 in the auricle of the Prrx1-CreERT; Bmpr1af/f mice compared to the control mice. Scale bars=50 μm. Arrows: positive signals.
G. WB blot also showed that H89 rescued the expression of the osteoblast marker genes Runx2 and osteocalcin in the mutant mice. Right panel: quantitation data. N=3. One-way ANOVA (and nonparametric or mixed) multiple comparisons were applied to evaluate the correlation data in (C, D, and G). p<0.05 was considered as statistically significant.