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Comparative transcriptomics reveals conserved and divergent hormone-responsive programs in primate endometrial organoids [mouse]

ABSTRACT: The epithelium of the uterine endometrium is a crucial interface with roles in uterine fluid production, defence against pathogens, and in the maternal-embryonic crosstalk necessary to embryo implantation. Mechanisms of embryo implantation are highly variable between mammals, and this phenomenon is thought to be partly controlled by maternal epithelial receptivity signals triggered by hormonal exposure. However, how endometrial epithelial cells and their hormone response pathways have functionally changed across mammals remains largely unknown. Here, we demonstrate that endometrial epithelial organoids are a promising hormone-responsive model to explore the contributions of endometrial epithelial cells to the evolution of mammalian reproductive innovations. By comparing transcriptomic responses to ovarian hormones in endometrial organoid models, we investigated how gene expression differs in endometrial epithelial cells between human, macaque and mouse at key time points in the hormonal cycle. Our results show that endometrial epithelial organoids faithfully reproduce species differences in cell differentiation programs, as well as gene expression specificities that may underlie phenotypic differences. In particular, we discovered that many maternal genes involved in uterine receptivity to embryo implantation exhibit divergent expression patterns between human, macaque and mouse, providing a molecular framework to explore primate- and human-specific traits in embryo implantation mechanisms.

ORGANISM(S): Mus musculus

PROVIDER: GSE286078 | GEO | 2026/09/07

REPOSITORIES: GEO

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Project description:Background: Recurrent implantation failure (RIF) remains a major barrier to successful assisted reproductive technology, given the lack of effective, mechanism-informed interventions to enhance endometrial receptivity. Jiawei Shoutai Wan (pills) (JWSTW), a modified formulation of the classic Shoutai Pill (STP) used in reproductive medicine, has not been systematically evaluated in the treatment of RIF, and its bioactive components and molecular targets remain largely unclear. Purpose: To determine whether JWSTW improves implantation competence and to identify the pathways associated with its effects. Materials and methods: A mifepristone-induced embryo implantation dysfunction (EID) rat model was established to evaluate implantation outcomes, uterine histology, and markers of endometrial receptivity and vascular perfusion. Bulk uterine transcriptomics and peripheral blood serum untargeted metabolomics were integrated with liquid chromatography-tandem mass spectrometry (LC-MS) based component profiling, network pharmacology, multi-omics correlation analysis, uterine cavity microbiota profiling and structure-based computational analyses. Key pathway molecules were further assessed using targeted molecular experiments. A retrospective cohort of RIF patients undergoing assisted reproduction was analyzed for ultrasound-derived endometrial receptivity parameters before and after treatment. Results: JWSTW administration improved implantation outcomes in EID rats, characterized by the upregulation of multiple receptivity- and perfusion-associated tissue markers. Integrated multi-omics analyses identified peroxisome proliferator-activated receptor (PPAR) signaling and lipid metabolism as significantly enriched pathways, supported by corresponding gene-metabolite correlations. JWSTW was also associated with structured changes in the uterine cavity microbiota, with enriched taxa and predicted functions aligned with lipid metabolism related pathways. LC-MS/MS characterization identified sweroside and loganic acid as major circulating constituents, while computational analyses prioritized a PPAR-centered target network with favorable binding affinity and structural stability. In the retrospective RIF cohort (n = 100), JWSTW was associated with increased endometrial thickness and improved Doppler-derived perfusion indices. Conclusion: These findings support JWSTW as a mechanism-informed candidate to improve endometrial receptivity in implantation failure via a PPAR-lipid metabolism axis.

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Comparative transcriptomics reveals conserved and divergent hormone-responsive programs in primate endometrial organoids [mouse]

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