Soybean Estrogen Impacts Cellular Function In Juvenile Rodent Testis

Overview

Background: Sertoli cells (SCs) play an important role in the development and function of the testes and in the process of spermatogenesis (generation of sperm). They are nurse cells, which provide structural and nutritional support to developing germ cells in the male gonad. SCs express estrogen receptors ERα and ERβ and the G-protein coupled estrogen receptor (GPER). Genistein (GEN), a phytoestrogen found in soy, mimics the effects of estradiol by binding to the estrogen receptors. The Culty lab previously found that genistein, an endocrine-disrupting chemical (EDC), dysregulates immature Sertoli cells development and function by downregulating key genes like Sox9 (essential for Sertoli cells development), Cox-1, Cox-2 (enzymes in the eicosanoid pathway) [1]. This in turn may interfere with testicular development and contribute to male infertility. In this experiment we aim to study which receptor genistein interacts with by co-treatment with the ESR1/2 antagonist, ICI 182 780 (ICI), or the GPER antagonist, G15 in immature rodent Sertoli cells. Methods: TM4 SCs were cultured and treated with genistein, ICI, G15, and their mixtures to see how they affect the cells. We used quantitative real-time PCR (qPCR) to measure the changes in gene expression, which gives us an idea of how the treatments alter the cells at the molecular level. In addition, immunofluorescence (IF) was utilized to study specific proteins such as Bcam and GP130 in the cells, giving us a more detailed insight into how the cells respond. We also worked with postnatal day (PND) 8 rat SCs as comparison. Results/Conclusion: Most treatments with genistein and receptor antagonists reduced Gp130 mRNA expression, with the greatest decrease seen in the GEN+ICI+G15 group. Immunofluorescent staining showed Bcam and Gp130 positive cell counts were mostly unchanged or slightly decreased across treatments.

Competition history

• CSEF 2026 Biochemistry/ Molecular Biology (Senior Division) · Entry S-04-08

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