Estradiol and progesterone regulate NUCB2/nesfatin-1 expression and function in GH3 pituitary cells and THESC endometrial cells

Abstract

Estradiol (E2) and progesterone (P4) are essential sex steroid hormones that play critical roles in the pituitary gland and uterus. Recently, nesfatin-1, a polypeptide hormone that regulates appetite and energy homeostasis in the hypothalamus, was found to be expressed in the pituitary gland and uterus. In this study, we aimed to investigate the relationship between these two steroid hormones and the expression and function of nesfatin-1 in the pituitary gland and uterus using GH3 cells, a lacto-somatotroph cell line, and THESC cells, an endometrial stromal cell line. First, we verified the presence of nesfatin-1 and nesfatin-1 binding sites in GH3 and THESC cells. E2 increased the mRNA expression of NUCB2, the gene encoding the nesfatin-1 protein, in GH3 cells, while P4 had no significant effect. In THESC cells, NUCB2 mRNA expression was decreased by E2 but increased by P4. In addition, nesfatin-1 significantly increased growth hormone (GH) and prolactin (PRL) mRNA expression in GH3 cells, and E2 enhanced this effect. In THESC cells, nesfatin-1 significantly increased the mRNA expression of insulin-like growth factor binding protein 1 (IGFBP1) and PRL, which are decidualization marker genes, and P4 further enhanced this effect. These results suggest that nesfatin-1 may act as a local regulator of GH and PRL production in the pituitary gland and decidualization in the uterus, modulating its effects in response to E2 and P4.

Generation of mouse and rat xenogeneic ovaries in vitro for production of mouse oocyte

“…One of the major diseases that causes female infertility, which affects about 1% of women aged 30–40 years old, is primary ovarian insufficiency (POI) or premature ovarian insufficiency (POF) (Sadeghi 2013 ; Torrealday et al 2017 ). In the reality that there are few effective methods of treating women with POI, hormone replacement therapy (a combination of estrogen, progestin, and gonadotropin) is the only standard treatment that replaces premenopausal levels of ovarian sex steroids (Luisi et al 2013 ; Park et al 2015 ; Kim et al 2022 ; Ha et al 2023 ). However, a fundamental way to overcome infertility is to uncover the mechanism of in vitro mammalian folliculogenesis and generate large numbers of in vitro oocytes.…”