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. 2020 Nov 24;4(22):5810–5824. doi: 10.1182/bloodadvances.2020003299

Figure 2.

Figure 2.

Embryonic PAR2 supports erythropoiesis in the fetal liver. (A) Fetal livers were collected from PAR2+/− and PAR2−/− embryos at E15.5, resulting from the mating of a PAR2+/− mother with a PAR2−/− father, and erythroid cell area was quantified on H&E-stained sections with ImageJ; scale bar, 50 µm. Each point in the graph is the average erythroid cell area from ≥8 field of views per mouse. (B-D) Fetal livers were collected at E13.5 from different timed mating strategies, and mRNA gene expression for erythroid master regulators and β-globin was normalized to r18s. Color coding indicate transcripts changed by maternal and embryonic PAR2 deficiency (beige bars), by only maternal PAR2 deletion (red bars), or by only embryonic PAR2 deletion (blue bars). (E) Expression of the indicated genes in fetal livers collected at E15.5 from WT/PAR2 R38E heterozygous embryos and from PAR2 R38E/PAR2 R38E homozygous embryos in PAR2 R38E/PAR2 R38E homozygous mothers or WT/PAR2 R38E heterozygous mothers. All data are mean ± standard deviation. *P < .05, **P < .01, ***P < .001, ****P < .0001, unpaired Student t test. Mann-Whitney U test was used for for KLF-1 (D) and Bcl-11a and KLF-1 (E, upper row).