Steroid hormone receptor profile of premenopausal endometrial polyps.

The etiology and pathogenesis of endometrial polyps (EPs) are only partially understood. To better understand how sex steroids regulate polyp growth, we investigated the messenger RNA (mRNA) expression of the genes of reproductive steroid hormone receptors (estrogen receptors alpha [ERalpha] and beta [ERbeta], G protein-coupled receptor 30 [GPR30], and progesterone receptor [PR]) in EP tissue and autologous normal appearing endometrium (R) Within each patient, the normal appearing endometrial tissue remote from the site of the endometrial polyp (R) was taken as an internal control. Relative expressions of genes of interest within the endometrial polyp were compared to expressions of respective genes within the internal control tissue (i.e. R). R is the abbreviation for normal appearing endometrium in the later calculation formula. Ten patients diagnosed with EP in a tertiary care center were included in this study. Directed biopsies were obtained under hysteroscopy from the EP and from a normal appearing site remote from EP along the opposite uterine wall in each patient. Quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) was used for gene expression profiling in the paired tissue samples. The relative gene expression between EP and normal appearing endometrium in each patient was analyzed with 2(-DeltaDeltaCt) method. We found that ERalpha, ERbeta, GPR30, and PR were expressed in both normal appearing endometrium and EP in each patient. ERalpha, ERbeta, GPR30, and PR showed no difference in relative expression in EP samples compared with paired normal endometrial samples from the same uterine cavity. However, the relative expression of PR correlated with that of GPR30 (r = .70, P = .023), suggesting that the co-expression of PR and GPR30 may be a contributory mechanism in the pathogenesis of EPs at least in a subset of women.