Progesterone Alleviates Endometriosis via Inhibition of Uterine Cell Proliferation, Inflammation and Angiogenesis in an Immunocompetent Mouse Model
Fig 5
Loss of ERα/PR-mediated signaling contributes to P4-resistance in this mouse model of endometriosis.
Endometriosis was induced and maintained with E2 as described in Fig 1. The host females were then treated with P4 beginning at 4 days before (Pre-) or 4 days after (Post-) endometrial cell transplantation until tissue collection (n = 6). Donor uterine tissue (D0) and ectopic lesions were subjected to IHC analysis (A) for ERα, PR and HAND2 protein expression (20X) or qPCR analysis (B) to assess expression level of mRNA corresponding to Esr1, Pgr, Hand2, and Hoxa10, respectively. (C) Lesion volumes were quantitated by 16 days after induction. The numerical values were analyzed by One-way ANOVA followed by Dunnett’s post hoc test and expressed as mean ± SEM. Statistical significance is defined as #: p < 0.05, *: p<0.01.