Mice Uterine Stem Cells are Affected by Neonatal Endocrine Disruption & Initiate Uteropathies in Adult Life Independent of Circulatory Ovarian Hormones

Pushpa Singh, Siddhanath Metkari, Siddhanath M Metkari, Deepa Bhartiya
Stem cell reviews and reports · 2021 · vol. 18(5) , pp. 1686–1701 · doi:10.1007/s12015-021-10279-8 · PMID:34750780 · W3211970867
article OA: closed CC0 ⤵ 3 in-corpus citations
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⚙ AI-generated summary by claude@2026-06+body, 2026-06-07 ⓘ

Neonatal endocrine disruption in mice directly alters uterine stem cells, leading to uteropathies in adulthood independent of circulating ovarian hormones, evidenced by hyperplasia and genomic instability.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This study examined whether developmental endocrine disruption alters uterine stem/progenitor cells to drive adult uteropathies. Mouse pups were exposed to estradiol or vehicle during postnatal days 3–7, then underwent bilateral ovariectomy at day 30 and received sequential estradiol/progesterone to induce a receptive uterus in controls; despite similar later hormonal exposure, endocrine disruption produced a non-receptive uterus with endometrial and myometrial hyperplasia, elevated stem cell marker expression (Oct-4A/Oct-4, Sox2, Nanog), poorly formed glands, and “defective” epithelial progenitors disseminated into the myometrium and blood vessels. The paper reports progesterone resistance and estradiol dominance via downregulation of Erα/Pr and upregulation of Erβ transcripts, alongside dysregulation of DNA mismatch repair/repair-axis transcripts and increased Ki67, which it interprets as genomic instability. A key caveat is that the mechanistic conclusions derive from marker and lesion analyses rather than direct functional lineage evidence. This paper is centrally about endometriosis — it links defective uterine epithelial progenitors arising from neonatal endocrine disruption to epithelial invasion/mobilization patterns consistent with initiation of endometriosis (and also adenomyosis) in adult life.

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mesh:D004715

MeSH descriptors

Adenomyosis Endometriosis Animals Embryonic Stem Cells Estradiol Estrogen Receptor alpha Estrogen Receptor alpha Estrogen Receptor beta Female Humans Hyperplasia Mice Pregnancy Progesterone Uterus

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