Abstract:

Objective To investigate the mechanism of changes of isoforms of local progesterone receptors (PRs) and 17β-hydroxysteroid dehydrogenase 2 (17β-HSD2) deficiency in insensitiveness of ectopic endometrium (EMT) to progestin. Methods Ectopic endometrium samples of 36 cases of EMT (EMT ectopic endometrium group) and 16 samples of eutopic endometrium (EMT eutopic endometrium group) were selected, the expression of PR-(A+B), PR-A, PR-B and 17β-HSD2 mRNA was detected by Real-Time PCR, and the expression of PR-(A+B), PR-B and 17β-HSD2 protein was determined by immunohistochemistry. Results In EMT eutopic endometrium group, the expression of PR-(A+B), PR-B and PR-A mRNA in proliferative phase was significantly higher than that in secretory phase (P＜0.05). PRs were expressed in both endometrial epithelial and stromal cells in proliferative phase, while those were mainly expressed in stromal cells in secretory phase. PR-A gained the advantage between PR-A and PR-B, while the rate of PR-A/PR-B was relatively stable during the whole menstrual cycle. The expression of PR-B in endometrial stromal cells was positively correlated with that of 17β-HSD2 in epithelial cells. In EMT ectopic endometrium group, the expression of PR-A was continuously low in the whole menstrual cycle, while there was no significant difference between the expression of PR-A in ectopic endometrium and that in eutopic endometrium in secretory phase (P＞0.05). The expression of PR-B in ectopic endometrium was significantly lower than that in eutopic endometrium in the whole menstrual cycle, and the cyclical variations of PR-A and PR-B disappeared in ectopic endometrium. Compared with EMT eutopic endometrium group, the expression of PR-B in EMT ectopic endometrium group was significantly lower, and the rate of PR-A/PR-B was significantly higher （P=0.001）. In EMT ectopic endometrium group, PR-B was significantly lower in stromal cells, 17β-HSD2 also decreased significantly, and the cyclical variation of 17β-HSD2 disappeared. Conclusion The changes of isoforms of PRs in ectopic endometrium may influence the expression of 17β-HSD2, which may be one of the mechanisms of progestin resistance for EMT.

Key words: endometriosis, ectopic endometrium, progesterone receptor isoforms, 17β-hydroxysteroid dehydrogenase 2, progestin resistance