Estrogen restricts the apoptosis of endometrial stromal cells by promoting TSLP secretion

Endometriosis (EMS) is a female hormone‑ dependent disease with controversial reports of its etiology and pathogenesis. Apoptosis is particularly important in the human endometrium due to the dynamic cycles of proliferation and shedding. Estrogen possessed antiapoptotic effects on endometrial stromal cells (ESCs), which appears to be exacerbated in women with EMS; however, the underlying mechanism of the antiapoptotic effects of estrogen on ESC remains unknown. The present study aimed to determine whether estrogen regulates the apoptosis of ESCs via thymic stromal lymphopoietin (TSLP) and the associated mechanism. An ELISA was conducted to detect TSLP content in the ESC culture medium treated with estrogen. Subsequently, the early apoptotic rate and expression of B‑cell lymphoma (Bcl‑2) of ESCs were analyzed by flow cytometry in the presence of recombinant human TSLP, anti‑human TSLP neutralizing antibody or estrogen. In the present study, it was reported that ESCs exhibited basal TSLP secretion in the absence of estrogen as reported in previous studies, and that estrogen promoted TSLP secretion of ESCs in a dose‑dependent manner. The results demonstrated that estrogen suppressed the apoptosis of ESCs associated with the promotion of Bcl‑2 expression, which may be partly reversed by inhibiting TSLP. Therefore, the findings of the present study revealed a novel mechanism of estrogen‑dependent apoptotic suppression of ESCs associated with TSLP secretion and Bcl‑2 regulation. Endogenous and estrogen‑induced endometrial TSLP may promote the initiation and development of EMS via the inhibition of apoptosis.