ArticleEndocrinology2024
A Dose-Response Study on Functional and Transcriptomic Effects of FSH on Ex Vivo Mouse Folliculogenesis.
Article in Endocrinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Review
- The Follicular Immune Checkpoint: PD-1/PD-L1 and Immune Tolerance in Oocyte Competence and IVF Failure.International journal of molecular sciences · 2026Review
- The BDNF/TrkB/CREB signaling improves chronic stress-induced decreased ovarian reserve by inhibiting pyroptosis of granulosa cells and disorders of sex hormone secretion.Journal of ovarian research · 2026Article
- Pituitary extract supplementation enhances follicular survival and gonadotropin receptor expression in vitrified ovarian tissue of Aceh cattle, Indonesia.Veterinary world · 2025Article
- Identification of FSH-regulated and estrous stage-specific transcriptional networks in mouse ovaries.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Unraveling the Clinical FSH Conundrum: Insights From the Small Ovarian Reserve Heifer Model.Molecular reproduction and development · 2025Review
- A Dose-Response Study on Functional and Transcriptomic Effects of FSH on Ex Vivo Mouse Folliculogenesis.Endocrinology · 2024Article
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Authors and funding
8 authors.
Funding
Abstract
Follicle-stimulating hormone (FSH) binds to its membrane receptor (FSHR) in granulosa cells to activate various signal transduction pathways and drive the gonadotropin-dependent phase of folliculogenesis. Both FSH insufficiency (due to genetic or nongenetic factors) and FSH excess (as encountered with ovarian stimulation in assisted reproductive technology [ART]) can cause poor female reproductive outcomes, but the underlying molecular mechanisms remain elusive. Herein, we conducted single-follicle and single-oocyte RNA sequencing analysis along with other approaches in an ex vivo mouse folliculogenesis and oogenesis system to investigate the effects of different concentrations of FSH on key follicular events. Our study revealed that a minimum FSH threshold is required for follicle maturation into the high estradiol-secreting preovulatory stage, and such threshold is moderately variable among individual follicles between 5 and 10 mIU/mL. FSH at 5, 10, 20, and 30 mIU/mL induced distinct expression patterns of follicle maturation-related genes, follicular transcriptomics, and follicular cAMP levels. RNA sequencing analysis identified FSH-stimulated activation of G proteins and downstream canonical and novel signaling pathways that may critically regulate follicle maturation, including the cAMP/PKA/CREB, PI3K/AKT/FOXO1, and glycolysis pathways. High FSH at 20 and 30 mIU/mL resulted in noncanonical FSH responses, including premature luteinization, high production of androgen and proinflammatory factors, and reduced expression of energy metabolism-related genes in oocytes. Together, this study improves our understanding of gonadotropin-dependent folliculogenesis and provides crucial insights into how high doses of FSH used in ART may impact follicular health, oocyte quality, pregnancy outcome, and systemic health.
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