Ectopic endometrial stromal cell-derived extracellular vesicles encapsulating microRNA-25-3p induce endometrial collagen I deposition impairing decidualization in endometriosis

Yuan Zhu, B. Zheng, Bo Zheng, Yuting Zhang, Mengyun Li, Yuan Jiang, Jidong Zhou, Yang Zhang, Nannan Kang, Min Wu, Yan Yuan, Jun Xing, Jianjun Zhou
Molecular human reproduction · 2024 · vol. 30(12) · doi:10.1093/molehr/gaae042 · PMID:39718837 · W4405737914
article OA: closed CC0 ⤵ 2 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-09 ⓘ

Ectopic endometrial stromal cell-derived extracellular vesicles, enriched with miR-25-3p, are preferentially taken up by eutopic stromal cells to increase collagen I deposition, impairing decidualization in endometriosis.

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Abstract

Endometrial collagen I undergoes dynamic degradation and remodelling in response to endometrial stromal cell (ESC) decidualization and embryo implantation. However, excessive collagen I deposition in the endometrium during the implantation window may impair decidualization, causing embryo implantation failure in patients with endometriosis (EMS). We found that endometrial collagen I expression during the mid-secretory phase was increased in the EMS group of patients. Collagen I stimulation resulted in decreased expression of the decidualization markers prolactin and insulin-like growth factor binding protein-1 in ESCs, impeding ESC transformation to a decidual morphology and decreasing the blastocyst-like spheroid expansion area in vitro. Treatment with extracellular vesicles (EVs) derived from the ectopic ESCs of EMS patients (EMS-EVs) increased collagen I expression in vivo and in vitro and decreased the blastocyst-like spheroid expansion area. Furthermore, EV microRNA (miRNA) sequencing revealed that there were 40 upregulated and 77 downregulated miRNAs in EMS-EVs when compared to the EVs derived from ESCs in the endometrium of control patients (CTL-EVs), including increased expression of miR-25-3p that targets phosphatase and tensin homolog (PTEN). We also found that PTEN expression was decreased and p-Akt expression was increased in the endometrium of EMS patients and EMS-EV-treated ESCs. miR-25-3p transfected ESCs exhibited increased collagen I, decreased PTEN, and increased p-Akt. Additionally, an EV uptake study further showed that EMS-EVs were preferentially taken up by ESCs rather than by endometrial epithelial cells. These results suggest that EMS-EVs encapsulating miR-25-3p might be preferentially taken up by eutopic ESCs where they may induce endometrial collagen I deposition to impair ESC decidualization in EMS.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Collagen Type I Collagen Type I Collagen Type I Collagen Type I Collagen Type I Collagen Type I Collagen Type I Collagen Type I Collagen Type I Collagen Type I Collagen Type I Collagen Type I Collagen Type I Collagen Type I Decidua Decidua Decidua Decidua Decidua Decidua

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Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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