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Objective. To determine whether bisphenol S (BPS), a common substitute for bisphenol A (BPA), induces cell proliferation and migration in human endometrial epithelial cells (Ishikawa) and adult mouse uterine tissues.Methodology. Human endometrial Ishikawa cells were exposed to low doses of BPS (1 nM and 100 nM) for 72 hours. Cell proliferation was assessed through the viability assays MTT and CellTiter-Glo ® . Wound healing assays were also used to evaluate the migration potential of the cell line. The expression of genes related to proliferation and migration was also determined. Similarly, adult mice were exposed to BPS at a dose of 30 mg/kg body weight/day for 21 days, after which, the uterus was sent for histopathologic assessment.Results. BPS increased cell number and stimulated migration in Ishikawa cells, in association with the upregulation of estrogen receptor beta (ESR2) and vimentin (VIM). In addition, mice exposed to BPS showed a significantly higher mean number of endometrial glands within the endometrium.Conclusion. Overall, in vitro and in vivo results obtained in this study showed that BPS could significantly promote endometrial epithelial cell proliferation and migration, a phenotype also observed with BPA exposure. Hence, the use of BPS in BPA-free products must be reassessed, as it may pose adverse reproductive health effects to humans.

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Intraperitoneal injection of endometrial tissues into inbred mice such as C57BL/6J is widely used as a model to study endometriosis, a disease characterized by the abnormal proliferation of endometrial cells which invade various tissues within the peritoneal cavity. However, most of these inbred mouse strains have a weak immune system and are often ovariectomized, which is not reflective of the human population in general. Hence, this study used the ovary intact ICR mouse strain as a model to study the immune response during endometriosis development using a non-surgical syngeneic model with no estrogen supplementation. We showed that ICR mice developed ectopic endometrial tissues after 8 wk, but these were mostly necrotic. Reducing the induction period to 4 wk increased the number of ectopic tissues, and endometriotic lesions were also formed in 30% of the induced recipient mice, albeit with a relatively low incidence rate. Endometriotic lesions in ICR mice were also associated with fewer lesion-resident macrophages and lesser vascularization than in C57BL/6J mice. This is further supported by a significantly downregulated expression of genes involved in angiogenesis and M2 macrophage activity in ICR versus C57BL/6J donor endometrium. Conversely, inflammatory response genes were significantly upregulated in the endometrium of ICR versus C57BL/6J mice. Overall, these data implicate the role of inflammation in inhibiting the establishment of endometrial lesions in ICR mice and the involvement of macrophage in promoting endometriosis in C57BL/6J mice. The present work reports the establishment of endometriotic lesions in outbred ICR mice by a less invasive syngeneic intraperitoneal injection procedure.