Gene expression pattern predictive of human ovarian follicle development and maturation.

In Brief: Granulosa cells from small antral follicles (SFs; diameter <10 mm), collected at the end of controlled ovarian cycles, differ from large ovarian follicles (LFs; >16 mm) for their molecular signatures. SFs retain characteristic of early antral follicles and the ratio between follicle-stimulating hormone receptor (FSHR) and G protein-coupled receptor (GPER) discriminates between mature and immature-like follicles.

Abstract: Ovarian follicle maturation is regulated by a network of genes involved in cell growth, differentiation, oocyte selection, and steroidogenesis.

Trafficking of luteinizing hormone receptor directs the differential signal activation between luteinizing hormone and chorionic gonadotropin.

Luteinizing hormone (LH) and human choriogonadotropin (hCG) support distinct reproductive events via differential activation of the luteinizing hormone receptor (LHCGR). LH-mediated LHCGR trafficking is known to be key in activating and regulating its signal responses, yet whether LH and hCG differentially direct LHCGR trafficking is unknown. Bioluminescence resonance energy transfer (BRET) trafficking biosensors and high-resolution TIRF imaging demonstrated that LH induces rapid internalization and recycling via an APPL1-linked very early endosomal pathway, while hCG-mediated receptor trafficking and recycling is slower, and preferentially involves β-arrestins and accumulation in endocytic compartments positive for early and late endosomal markers.

Benzo[a]pyrene disrupts LH/hCG-dependent mouse Leydig cell steroidogenesis through receptor/Gαs protein targeting.

Steroidogenesis of gonadal cells is tightly regulated by gonadotropins. However, certain polycyclic aromatic hydrocarbons, including Benzo[a]pyrene (BaP), induce reproductive toxicity. Several existing studies have considered higher than environmentally relevant concentrations of BaP on male and female steroidogenesis following long-term exposure.

Short-Term Exposure to Bisphenol A Does Not Impact Gonadal Cell Steroidogenesis In Vitro.

Bisphenol A (BPA) is a ubiquitous, synthetic chemical proven to induce reproductive disorders in both men and women. The available studies investigated the effects of BPA on male and female steroidogenesis following long-term exposure to the compound at relatively high environmental concentrations. However, the impact of short-term exposure to BPA on reproduction is poorly studied.