DNA methylation is involved in regulation of PR-signaling in endometriosis.

Yanfen Li (3239550), Malavika K. Adur (3239547), Athilakshmi Kannan (483347), Juanmahel Davila (787251), Yuechao Zhao (1358766), Romana A. Nowak (457413), Milan K. Bagchi (181461), Indrani C. Bagchi (181462), Quanxi Li (181459)
2016 · doi:10.1371/journal.pone.0165347.g006 · W6904445182
other OA: green CC0
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This study investigated the role of progesterone receptor signaling in endometriosis using an immunocompetent mouse model where lesions were induced and maintained with estradiol. Researchers treated these mice with decitabine, a DNA methyltransferase inhibitor, to determine if DNA methylation regulates progesterone resistance within ectopic endometrial tissues. The findings demonstrated that inhibiting DNA methylation restored progesterone receptor expression and alleviated lesion growth by suppressing cell proliferation, inflammation, and angiogenesis. This paper is centrally about endometriosis, specifically focusing on the molecular mechanisms of progesterone resistance driven by DNA methylation in ectopic lesions.

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Abstract

Endometriosis was induced in female mice and maintained with E2. Beginning at 4 days after induction, host females were treated with either vehicle (VEH) or 0.5 mg/kg of Decitabine (DAC) intraperitoneally, once every other day until tissues collection (n = 6). (A) Lesion volumes were measured at 8 and 16 days after induction. (B) The eutopic endometrium (EU) and the ectopic lesions (EC) were subjected to IHC analysis for PGR protein expression (20X). Representative images from each group are shown. The relative intensities of PR staining were analyzed by ImageJ software. (C) qPCR was employed to analyze relative levels of gene expression in the ectopic lesions (D16) treated with VEH or DAC. (D) DNA methylation levels of Hoxa10 and Pgr promoters were assessed by qPCR following digestion of genomic DNA with methylation-specific enzymes. 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.
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Progesterone Alleviates Endometriosis via Inhibition of Uterine Cell Proliferation, Inflammation and Angiogenesis in an Immunocompetent Mouse Model Fig 6 DNA methylation is involved in regulation of PR-signaling in endometriosis. Endometriosis was induced in female mice and maintained with E2. Beginning at 4 days after induction, host females were treated with either vehicle (VEH) or 0.5 mg/kg of Decitabine (DAC) intraperitoneally, once every other day until tissues collection (n = 6). (A) Lesion volumes were measured at 8 and 16 days after induction. (B) The eutopic endometrium (EU) and the ectopic lesions (EC) were subjected to IHC analysis for PGR protein expression (20X). Representative images from each group are shown. The relative intensities of PR staining were analyzed by ImageJ software. (C) qPCR was employed to analyze relative levels of gene expression in the ectopic lesions (D16) treated with VEH or DAC. (D) DNA methylation levels of Hoxa10 and Pgr promoters were assessed by qPCR following digestion of genomic DNA with methylation-specific enzymes. 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.

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