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. 2020 Mar 3;130(4):1767–1781. doi: 10.1172/JCI133473

Figure 3. iPTH treatment fails to regulate SC proliferation and life span, T cell expression of Wnt10b, number of Tregs, and BM production of TGF-β and IGF-1.

Figure 3

(A and B) SC proliferation as measured by thymidine incorporation (n = 8–10 mice/group). (C and D) SC apoptosis as measured by Caspase-3 activity (n = 5 mice/group). (E and F) mRNA levels of bone sialoprotein (Bsp), type 1 collagen (Col1), osteocalcin (Ocn), osterix (Osx), and Runx2, which are factors representative of the differentiation of SCs into osteoblasts (n = 5 mice/group). (G and H) Transcripts of genes that are specifically increased by Wnt signaling in SCs. The analyzed genes were aryl-hydrocarbon receptor (Ahr), Axin2, cysteine rich protein 61 (Cyr61), naked cuticle 2 homolog (Nkd2), transgelin (Tagln), transforming growth factor β3 (Tgfb3), thrombospondin 1 (Thbs1), Wnt1 inducible signaling pathway protein 1 (Wisp1), and Twist gene homolog 1 (Twist1) (n = 5 mice/group). (I–L) Wnt10b mRNA levels in whole BM cells and sorted BM CD8+ T cells (n = 5 mice/group). (M–P) PP and BM Tregs (TCR-β+CD4+Foxp3+ cells) (n = 8–10 mice/group). (Q and R) BM Tgfb1mRNA levels (n = 5 mice/group). (S and T) BM Igf-1 mRNA levels (n = 5 mice/group). Data were expressed as mean ± SEM. All data were normally distributed according to the Shapiro-Wilk normality test. All data were analyzed by 2-way ANOVA and post hoc tests, applying Bonferroni’s correction for multiple comparisons. **P < 0.01, ***P < 0.001, and ****P < 0.0001 compared with the indicated group in the post hoc tests.