Promoter Hypermethylation of Progesterone Receptor Isoform B (PR-B) in Endometriosis

Yan Wu, Wu Y, Strawn E, Estil Strawn, Zainab Basir, Basir Z, Gloria Halverson, Halverson G, Sun-Wei Guo, Sun‐Wei Guo, Guo SW
Epigenetics · 2006 · vol. 1(2) , pp. 106–111 · doi:10.4161/epi.1.2.2766 · PMID:17965625 · W1998290637
article OA: bronze CC0 ⤵ 221 in-corpus citations
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The PR-B promoter region is hypermethylated in endometriosis, leading to reduced PR-B expression and potentially contributing to progesterone resistance.

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Abstract

The physiological effects of progesterone (P) are mediated by two isoforms of progesterone receptors (PRs): PR-A and PR-B. Progestins have long been used in the treatment of endometriosis but unfortunately the relief of pain is relatively short-term. In addition, about nine percent of women with endometriosis simply do not respond to progestin therapy due to unknown reasons. In fact, a general tendency for relative progesterone resistance within eutopic and ectopic endometrium of women with endometriosis and also the downregulation of PR-B, but not PR-A, in endometriosis have been noted. Since promoter hypermethylation is well-documented to be associated with transcriptional silencing, we sought to determine the methylation status of the PR-A and PR-B promoter regions in the epithelial component of endometriotic implants using a combination of laser capture microdissection (LCM), methylation specific PCR, and bisulfite sequencing. We found that the promoter region of PR-B, but not PR-A, is hypermethylated in endometriosis as compared with controls. In addition, the PR-B expression was significantly reduced in the ectopic endometrium. Our finding suggests that progesterone resistance in endometriosis in general and the down regulation of PR-B, but not PR-A, in particular, are a result of promoter hypermethylation of PR-B, but not PR-A. This, in conjunction with our reported aberrant methylation of HOXA10 in the eutopic endometrium of women with endometriosis, strongly suggests that endometriosis is an epigenetic disease. This perspective should potentially open up new avenues for the delineation of pathogenesis of endometriosis, and might also lead to novel ways to treat the disease through reversing aberrant methylation via pharmacological means.

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Condition tags

endometriosis

MeSH descriptors

DNA Methylation Endometriosis Ovarian Diseases Peritoneal Diseases Promoter Regions, Genetic Promoter Regions, Genetic Receptors, Progesterone Adolescent Adult Base Sequence Case-Control Studies Down-Regulation Drug Resistance Drug Resistance Endometriosis Endometriosis Female Humans Molecular Sequence Data Ovarian Diseases

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