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. Author manuscript; available in PMC: 2017 Mar 6.
Published in final edited form as: Cell Rep. 2016 Oct 4;17(2):458–468. doi: 10.1016/j.celrep.2016.09.012

Figure 2. 1,25(OH)D3 Regulates HSPC Numbers via Vitamin D Receptor Signaling.

Figure 2

(A) Representative runx1/cmyb WISH images and qualitative phenotype distribution following 25(OH)D3 exposure from 12–36 hpf (n ≥ 40 embryos/condition).

(B) FACS analysis of 25(OH)D3-treated (10 µM) embryos showed a significant increase in HSPCs (**p < 0.01) (5 embryos/sample 3 4 replicates/condition). Error bars, mean ± SD.

(C) qPCR analysis indicated a significant induction in the VDR transcriptional target cyp24a1 at 36 hpf after exposure to 25(OH)D3 (*p < 0.05) or 1,25(OH)D3 (***p < 0.001) (12–36 hpf) (30 pooled embryos/condition 3 3 replicates).

(D) Phenotype distribution of runx1/cmyb expression in embryos exposed to increasing concentrations of 1,25(OH)D3 from 12–36 hpf (n ≥ 30 embryos/condition).

(E) FACS analysis of 1,25(OH)D3-treated (10 mM) embryos showed a 20% increase in HSPCs at 48 hpf (**p < 0.01) compared with controls (n value and error bars as in B).

(F) runx1/cmyb WISH and phenotype distribution after exposure to the non-calcemic vitamin D3 analog calcipotriol (n ≥ 30 embryos/condition).

(G) FACS analysis of calcipotriol-treated embryos showed a significantly more HSPCs (*p < 0.05) at 36 hpf (n value and error bars as in B). Scale bars, 100 µm. See also Figure S2.