A novel role of follicle-stimulating hormone (FSH) in various regeneration-related functions of endometrial stem cells

Se-Ra Park, Soo‐Rim Kim, Seong‐Kwan Kim, Jeong-Ran Park, In‐Sun Hong
In: Experimental & Molecular Medicine · 2022 · vol. 54(9) , pp. 1524–1535 · doi:10.1038/s12276-022-00858-1 · PMID:36117220 · W4296329016
article OA: gold CC0 ⤵ 2 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This study found that follicle-stimulating hormone (FSH) inhibits endometrial stem cell self-renewal, migration, and differentiation via PI3K/Akt and ERK1/2 signaling pathways.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-10 ⓘ

This paper investigated whether follicle-stimulating hormone (FSH) can directly impair regeneration-related functions of human endometrial stem cells, motivated by the low pregnancy outcomes seen with prolonged FSH use in assisted reproductive technologies. Using human endometrial stem cells isolated from uterine fibroid patients, the authors assessed FSH effects on proliferation, migration, and multilineage differentiation after FSH exposure in vitro, and examined underlying signaling changes in vitro and in vivo, focusing on PI3K/Akt and ERK1/2 pathways, with FSH receptor (FSHR) knockdown used to test FSHR involvement. They found that FSH inhibited endometrial stem cell self-renewal-associated behavior, migration, and adipogenic/osteogenic differentiation capacities via PI3K/Akt and ERK1/2 signaling both in vitro and in vivo. A key limitation stated by the study context is that endometrial stem cells were derived from fibroid patients rather than people undergoing FSH-based ART, which may affect generalizability. This paper is centrally about endometriosis — it does not explicitly discuss endometriosis but is included in the corpus due to its direct relevance to endometrial stem cell biology and FSH-mediated effects on endometrial regeneration, which are mechanisms considered in endometriosis research.

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Abstract

Follicle-stimulating hormone (FSH) promotes the production and secretion of estrogen, which in turn stimulates the growth and maturation of ovarian follicles. Therefore, consecutive FSH treatment to induce ovarian hyperstimulation (superovulation) is still considered the most cost-effective option for the majority of assisted reproductive technologies (ARTs). However, a relatively high cancellation rate and subsequent low pregnancy outcomes (approximately 15%) are the most challenging aspects of this FSH-based ART. Currently, the main cause for this low implantation rate of FSH-based ART has not yet been revealed. Therefore, we hypothesized that these high cancellation rates with FSH-based superovulation protocols might be associated with the harmful effects of consecutive FSH treatment. Importantly, several recent studies have revealed that tissue-resident stem cell deficiency can significantly reduce cyclic endometrial regeneration and subsequently decrease the pregnancy outcome. In this context, we investigated whether FSH treatment could directly inhibit endometrial stem cell functions and consequently suppress endometrial regeneration. Consistent with our hypothesis, our results revealed for the first time that FSH could inhibit various regeneration-associated functions of endometrial stem cells, such as self-renewal, migration, and multilineage differentiation capacities, via the PI3K/Akt and ERK1/2 signaling pathways both in vitro and in vivo.

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