Fig. 7: Detection of retinoid- and BMP-signaling pathways in control and Smad2/3 cKO mice.
From: SMAD2/3 signaling in the uterine epithelium controls endometrial cell homeostasis and regeneration
a–d Cross-sections from 17-week-old control (a, b) and Smad2/3 cKO (c, d) mice stained with ALDH1A1 antibody. ALDH1A1 is enriched in the crypts of the mouse endometrial glands. e–h ALDH1A2 IHC in the uteri of control (e, f) and Smad2/3 cKO mice (g, h) ALHD1A2 is localized to the subepithelial stromal compartment. i–l ALDH1A3 IHC in control (I, j) and Smad2/3 cKO (k, l) mice shows enrichment in the crypts of endometrial glands. m–p pSMAD2 IHC in control (m, n) and Smad2/3 cKO (o, p) uterine cross-sections. Decreased pSMAD2 is observed in Smad2/3 cKO mice. q–t pSMAD1/5 IHC in the uterine cross-sections of control (q, r) and Smad2/3 cKO (s, t) mice shows increased pSMAD1/5 reactivity in the uteri of Smad2/3 cKO mice. IHC experiments were performed in >3 mice per genotype. u Quantitative PCR analysis of uterine epithelium from control (n = 4) and Smad2/3 cKO (n = 6) for genes involved in retinoid signaling (Cyp26a1, Aldh1a1, -1a2, -1a3, Lrat, and Rbp4) or BMP signaling (Id1, Id2, Id3, Id4). Histograms represent mean ± SEM analyzed by an unpaired two-tailed t-test.
