Divergent expression of two prostaglandin E receptors (EP1 and EP3) in normal endometrium (NE) and in ectopic endometriosis lesions of ovarian origin (EC)

Implantation and endometriosis are the results of intricate interactions of hormones, prostaglandins and cytokines designating tissues to adhesion, migration and apoptosis. EP1 and EP3 have been implicated in promoting these processes. Although the crucial role of prostaglandins in diverse physiological and pathological processes is known, the effects of their receptors on implantation and endometriosis remain to be elucidated. Here we investigate the expression levels of prostaglandin receptors in NE and EC. Study design: Normal endometrial tissues of 46 patients from at all phases of the menstrual cycle as well as ectopic endometrial tissues from 15 endometriosis patients were included.

Samples were stained by immunohistochemistry, using anti-EP1 and anti-EP3 antibodies. Staining intensity was analyzed with a semi-quantitative assay (IRS).

EP1 expression of both glandular cells (P < 0.001) and stromal cells (p < 0.05) is significantly higher in NE during the proliferative phase compared to the early secretory phase. EP1 expression of glandular cells is also significantly higher in EC (P < 0.001) In contrast, analysis of EP3 expression revealed the exact opposite pattern: EP3 expression of NE was significantly lower in glandular cells during the proliferative phase compared to the early secretory phase (P < 0.05) and in EC (P < 0.05).

While EP1 expression decreases during the window of implantation in NE and increases in EC, EP3 expression behaves in the opposite way. The mutually oppositional changes of EP1 and EP3 expression hint at a tightly orchestrated regulation to facilitate implantation and a possible role in the pathophysiology of endometriosis.