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

Lab / animal OA: closed CC0 ⤵ 2 in-corpus citations
View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 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.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

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.

My notes (saved in your browser only)

Condition tags

endometriosis

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 Collagen Type I Collagen Type I Collagen Type I Collagen Type I Collagen Type I Collagen Type I

Citation neighborhood (2-hop)

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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (38)

Cited by (2)

Source provenance

europepmc
last seen: 2026-10-14T06:08:39.101224+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-10-14T06:06:03.711037+00:00
unpaywall
last seen: 2026-10-14T06:23:58.021457+00:00
License: CC0 · commercial use OK