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Endometriosis-derived iPSCs reveal conserved stromal maturation and endocrine responsiveness

ABSTRACT: Endometriosis is a chronic, hormone-dependent disease characterized by altered endometrial stromal function, yet mechanistic and translational studies have been limited by the lack of tractable human model systems. Here, we establish an induced pluripotent stem cell (iPSC)–based platform derived from patients with endometriosis to model endometrial stromal differentiation in a controlled human context. Using a defined differentiation framework, endometriosis-derived iPSCs transition from pluripotency through mesenchymal commitment toward stromal-like states and acquire transcriptional hormone responsiveness. Trajectory-resolved transcriptomic analyses reveal coordinated repression of pluripotency and proliferative programs with induction of stromal lineage signatures. Benchmarking against independent bulk transcriptomic datasets demonstrated that in vitro–derived stromal cells progressively acquired gene expression profiles that resembled eutopic endometrial stromal programs in endometriosis. To explore potential functional consequences, conditioned media from iPSC-derived stromal cells was applied to THP-1 macrophage-like cells, revealing coordinated transcriptional reprogramming. Together, these results establish a patient-derived platform for modeling stromal differentiation and hormone responsiveness in a disease-relevant context. While this model captures key features of stromal identity, definitive assessment of disease-specific phenotypes will require future studies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE328997 | GEO | 2026/08/26

REPOSITORIES: GEO

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Project description:Background Reduced endometrial receptivity is a major factor for impaired fertility in endometriosis (EMS). Endometrial deposition of collagen I proteins may account for poor endometrial receptivity in endometriosis. Methods We investigated the expression of collagen I expression in endometrium of endometriosis patients and in constructed EMS mice model. Effect of collagen I on ESCs was evaluated. Co-culture of exosomes with ESCs was conducted to evaluate the uptake of exosomes by different endometrial cell lines and the effect on decidualization of eutopic ESCs and embryo implantation. MiRNA expression profiles were compared between ectopic ESC derived exosomes and eutopic ESC derived exosomes. Luciferase reporter and its mutant plasmids were applied to confirm the direct target of miR-25-3p. Findings Here we found endometrial collagen I deposition with impaired decidualization in endometriosis patients and EMS mice model. Treatment of collagen I with ESCs contributed to impaired decidualization and inhibited BLS expansion in vitro. Endometriotic stromal cell-derived exosomes were detected in eutopic endometrium and the ectopic endometrial stromal cell derived exosomes were more taken-up by the same cell line in eutopic endometrium. Treatment of endometriotic stromal cell-derived exosomes increased the expression of endometrial collagen I in vitro and in vivo, while inhibited BLS expansion. Exosomal miR-25-3p was significantly increased in endometriotic stromal cell-derived exosomes compared with control group, and PTEN is a certain target of miR-25-3p. The promotion of endometrial miR-25-3p significantly increased collagen I expression in vitro through the PTEN/Akt pathway. Interpretation These results suggested that endometriotic stromal cell-derived exosomal miR-25-3p played key role in inducing endometrial collagen I deposition to impair embryo expansion in endometriosis via PTEN/Akt pathway. Funding National Nature Science Foundation of China (82271702), National Natural Science Foundation of China (81771537). Keywords: endometriosis; exosome; collagen I; miRNA; collagen deposition

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Endometriosis-derived iPSCs reveal conserved stromal maturation and endocrine responsiveness

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