Figure 5. Decidual senescence persists in uteri deleted of Trp53.

(A and B) Number and weight of implantation sites in Trp53^loxP/loxPPgr^+/+ and Trp53^loxP/loxPPgr^Cre/+ mice on day 16 of pregnancy (mean ± SEM; *P < 0.05). (C) Uterine loss of p53 impeded decidual growth. Placental labyrinth and spongiotrophoblast layers were demarcated by cytokeratin-8 immunostaining. (D) Uterine Trp53 deletion enhanced SA–β-gal activity primarily in the decidual layer on days 12 and 16. (C and D) Decidual boundaries are demarcated by double-sided arrows. Myo, myometrium; Dec, decidua; Sp, spongiotrophoblast; Lb, labyrinth; BV, blood vessel. Scale bars: 500 μm. (E and F) Levels of p21, pAkt, and p110α were upregulated in day 16 uteri lacking p53. (E) Uterine samples from which placentas and fetuses had been removed were used for Western blotting. (F) Quantitative analysis of band intensities of pAkt were normalized against total Akt, and those of p21 and p110α were normalized against actin (mean ± SEM; *P < 0.05). In each group, 3 independent samples from different mice were examined. (G) Serum levels of E₂ and P₄ (mean ± SEM; P > 0.05). At least 4 independent samples were examined in each group. (H) Representative photomicrographs of H&E-stained histological sections of ovaries on day 16 of pregnancy. CL, corpus luteum; F, follicle. Scale bar: 200 μm. (I) Western blotting of ovarian 20α-HSD levels on day 16 of pregnancy. Day-20 WT mice were used as a positive control. (J) Quantitative analysis of 20α-HSD band intensities from I were normalized against actin (mean ± SEM; P > 0.05).