PCOS Influences the Expression of AMHRII in the Endometrium of AEH During the Reproductive Age.

BACKGROUND

Endometrial proliferative lesions (EPLs) encompass endometrial hyperplasia (EH) and endometrial carcinoma (EC). Atypical endometrial hyperplasia (AEH) is associated with an elevated risk of progression to EC. Patients with polycystic ovarian syndrome (PCOS) exhibit higher serum levels of anti-Müllerian hormone (AMH) and a correspondingly increased incidence of EPLs. AMH has the capacity to inhibit the cell proliferation of EPLs derived from Müllerian duct tissue through the AMH-AMH receptor (AMHR) signaling pathway.

METHODS

Pairs of samples matched by preference scores were randomly selected. Immunohistochemistry was employed to assess the expression levels of AMHR type II (AMHR2) in endometrial tissue. A comparative analysis was performed between tissues from individuals with PCOS and those without, as well as between a normal endometrium and endometrial tissue from individuals with EPLs. This study aimed to elucidate differences in AMHR2 expression among these tissue types. By focusing on AMHR2 expression, the impact of the PCOS-related background on the endometrial AMH-AMHR cascade signaling pathway was initially investigated.

RESULTS

The AMHR2 protein was expressed in the endometrium of both the PCOS group and the non-PCOS group during the reproductive age (20-39 years). The expression of the AMHR2 protein in the AEH endometrium of PCOS patients did not differ significantly from that in the normal endometrium of PCOS patients; however, it was significantly higher than in the AEH endometrium of non-PCOS patients ( = 0.011). Conversely, the expression of the AMHR2 protein in the AEH endometrium of non-PCOS patients was significantly lower than that in the normal endometrium of non-PCOS patients ( = 0.021). Notably, there was no significant difference in AMHR2 protein expression in a normal endometrium between PCOS and non-PCOS patients.

CONCLUSIONS

The involvement of the endometrial AMH-AMHR cascade signaling pathway and its biological effects in the pathogenesis of AEH are evident. The pathophysiological conditions associated with PCOS, such as elevated serum AMH levels and other pathological states, may directly or indirectly influence the AMH-AMHR cascade signaling pathway in the endometrium. This influence could contribute to the progression of AEH.