Endometriosis is one of the most frequent gynecological diseases in reproductive age women, but its etiology is not completely understood. Endometriosis is characterized by progesterone resistance, which has been explained in part by a decrease in the expression of the intracellular progesterone receptor in the ectopic endometrium. Progesterone action is also mediated by nongenomic mechanisms via membrane progesterone receptors (mPRs) that belong to the class II members of the progesterone and adipoQ receptor (PAQR) family. The aim of the present study was to evaluate the expression at mRNA and protein levels of mPR members in the eutopic and ectopic endometrium of women with endometriosis. Total RNA and total protein were isolated from control endometrium (17 samples), eutopic endometrium (17 samples), and ectopic endometrium (9 samples). The expression of PAQR7 (mPRα), PAQR8 (mPRβ), and PAQR6 (mPRδ) at mRNA and protein levels was evaluated by RT‐qPCR and Western blot, whereas PAQR5 (mPRγ) gene expression was evaluated by RT‐qPCR. Statistical analysis between comparable groups was performed using one‐way ANOVA followed by Tukey’s multiple comparisons test with a confidence interval of 95 %. The analysis of gene expression showed that PAQR7 and PAQR5 expression was lower in both eutopic and ectopic endometrium as compared to the endometrium of women without endometriosis, whereas the expression of PAQR8 and PAQR6 was only reduced in eutopic endometrium. Furthermore, mPRα and mPRβ protein content was decreased in the ectopic endometrium of women with endometriosis. Our results demonstrate a decrease in the expression and protein content of mPRs in eutopic and ectopic endometrium of patients with endometriosis, which could contribute to the progesterone resistance observed in patients with this disease.

Endometriosis is a disorder characterized by the presence of endometrial tissue outside the uterus, leading to dyspareunia, chronic pelvic pain, dysuria, and infertility. The latter has been related to implantation failure associated with alterations in decidualization, a process regulated by sex hormones such as progesterone. Membrane progesterone receptor β (mPRβ) exhibits a lower expression in endometriotic tissues than in normal endometrial ones. However, the role of mPRβ in decidualization is unknown. This work aimed to investigate whether mPRβ plays a role in the decidualization of endometrial stromal cells (ESCs) derived from women with and without endometriosis. The mPR agonist OrgOD-2 induced the gene expression of key decidualization markers (insulin-like growth factor binding protein 1, prolactin, transcription factor heart and neural crest derivatives-expressed transcript 2, and fork-head transcription factor) in healthy ESCs, eutopic (uterine cavity), and ectopic (outside of the uterine cavity) ESCs from women with endometriosis. Notably, the expression of the decidualization markers was lower in endometriotic cells than in healthy endometrial ones. An siRNA mediated knockdown of mPRβ reduced the expression of decidualization-associated genes in ESCs treated with a decidualization stimuli, regardless of whether cells were derived from healthy women or those with endometriosis. Our data suggest that progesterone, through mPRβ activation, regulates the decidualization process in endometrial stromal cells from women with and without endometriosis.

Background/Objective: Asherman syndrome is an acquired intrauterine adhesive disorder associated with menstrual abnormalities, infertility, recurrent pregnancy loss, and adverse reproductive outcomes. Data from Latin American tertiary referral centers remain limited. To characterize clinical history, classification, hysteroscopic management strategies, and anatomical and reproductive outcomes in a single cohort of Mexican women with Asherman syndrome. Methods: This retrospective cohort study included women identified through institutional electronic records between July 2016 and December 2023 with a diagnosis of Asherman syndrome and analyzable hysteroscopic records. Women were followed for twelve months. Recurrence was defined as hysteroscopic evidence of intrauterine adhesions during follow-up. Among women with follow-up hysteroscopy, two-sided Fisher’s exact tests were used to calculate odds ratios and 95% confidence intervals. Results: Fifty-four women were analyzed. A prior uterine procedure was documented in 44 women (81.5%), with sharp curettage in 35 (64.8%). The most common reasons for consultation were secondary infertility (29.6%), abnormal uterine bleeding (27.8%), primary infertility (20.4%), and recurrent pregnancy loss (13.0%). Disease severity was classified as mild in 30 women (55.6%), moderate in 11 (20.4%), and severe in 7 (13.0%). Hysteroscopic intervention was predominantly performed with cold knife adhesiolysis (83.3%). Twelve-month follow-up hysteroscopy was performed in 38 women (70.4%); recurrence was identified in 30 (55.6%). Among the 34 women with reproductive intent, 12 achieved a live birth, corresponding to a live birth rate of 35.3%. Conclusions: Prior uterine instrumentation, particularly sharp curettage, was the most frequent antecedent. Recurrence remained common despite surgical management, highlighting the need for standardized postoperative surveillance and preventive strategies.