A novel rat model of ovarian endometrioma: single-cell RNA sequencing reveals its impact on ovarian function
Lab / animal
OA: gold
CC0
AI-generated summary
A rat model of ovarian endometrioma demonstrated that single-cell RNA sequencing reveals disrupted granulosa cell differentiation, stromal fibrosis, and immune dysregulation as mechanisms underlying OEM-induced ovarian functional decline.
One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works
AI-generated deep summary
Researchers established a rat model of ovarian endometrioma by suturing homologous endometrial tissue onto the ovarian surface to investigate mechanisms of ovarian dysfunction. Single-cell RNA sequencing and histological analyses revealed that this condition disrupts estrous cycles, alters serum hormone levels, and induces significant changes in ovarian cellular composition, including granulosa cell dysfunction and stromal fibrosis. The study identified synergistic effects involving immune dysregulation, specifically increased T cells and neutrophils, alongside enhanced inflammatory signaling pathways that contribute to functional decline. This paper is centrally about endometriosis — specifically focusing on the pathological mechanisms and cellular landscape of ovarian endometrioma lesions.
Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works
Abstract
Abstract Background Ovarian endometrioma (OEM) is a leading cause of infertility in women of reproductive age; however, the cellular and molecular mechanisms by which it impairs ovarian function remain poorly understood. Direct investigation of OEM-induced ovarian dysfunction is hampered by the difficulty in obtaining clinical ovarian tissue samples, and the lack of stable animal models that faithfully simulate the pathological features of human OEM represents a critical bottleneck in this field. Methods A rat model of OEM was established by suturing homologous rat endometrial tissue onto the ovarian surface. The impact of OEM on ovarian function was evaluated through the estrous cycle, serum hormone levels, and histopathological staining. Single-cell RNA sequencing (scRNA-seq) was employed to analyse ovarian tissue from the OEM group and the control group, with the aim of mapping cellular landscapes, identifying the composition of cell subpopulations, conducting differential gene enrichment analyses, and characterising changes in differentiation trajectories and intercellular communication networks. Key phenotypic findings were further validated through histopathological staining, immunofluorescence, Real-time Reverse Transcription PCR, and Western blot. Results A rat model of OEM was successfully established by suturing homologous rat endometrial tissue onto the ovarian surface. Estrous cycle monitoring revealed disrupted estrous cycles in OEM model rats. ELISA demonstrated significantly decreased serum AMH and E2 levels, accompanied by elevated FSH levels in the OEM group. CD10 immunostaining confirmed the positive expression of endometrial tissue, and Prussian blue staining revealed markedly increased iron deposition in the OEM group ovaries. The scRNA-seq identified a total of 70,041 cells, revealing seven major cell types. OEM significantly altered the cellular composition of the ovary, with decreased proportions of granulosa and endothelial cells and an increased overall proportion of immune cells; within the immune-cell compartment, the proportions of macrophages and B cells decreased, whereas those of T cells and neutrophils increased. Granulosa cell analysis revealed disrupted differentiation trajectories, attenuated intercellular AMH and Estradiol signaling, and significantly downregulated mRNA and protein expression of AMH, FSHR, and ESR2 in the OEM group. Stromal cell analysis demonstrated significant enrichment of TGF-β and collagen signaling pathways, with upregulated mRNA and protein expression of COL1A1, TGFB1, and ACTA2 in the OEM group. Masson’s trichrome and Sirius Red staining confirmed significantly increased fibrotic areas in the OEM group ovaries. Immune cell analysis revealed significant enrichment of chemokine signaling and IL-17 signaling pathways, enhanced CCL and CXCL chemokine communication networks, and upregulated mRNA and protein expression of inflammatory mediators, including CXCL1, CCL2, and IL1b in the OEM group. Conclusions This study successfully established a rat model that simulates the key pathological features of OEM. Utilizing scRNA-seq, we constructed, for the first time, a comprehensive cellular landscape of the OEM-affected ovary, revealing the synergistic effects of granulosa cell dysfunction, ovarian stromal fibrosis, and immune dysregulation in OEM-induced ovarian functional decline.
Full text
5,620 characters
· extracted from
oa-html
· 5 sections
· click to expand
Abstract
Background
Ovarian endometrioma (OEM) is a leading cause of infertility in women of reproductive age; however, the cellular and molecular mechanisms by which it impairs ovarian function remain poorly understood. Direct investigation of OEM-induced ovarian dysfunction is hampered by the difficulty in obtaining clinical ovarian tissue samples, and the lack of stable animal models that faithfully simulate the pathological features of human OEM represents a critical bottleneck in this field.
Methods
A rat model of OEM was established by suturing homologous rat endometrial tissue onto the ovarian surface. The impact of OEM on ovarian function was evaluated through the estrous cycle, serum hormone levels, and histopathological staining. Single-cell RNA sequencing (scRNA-seq) was employed to analyse ovarian tissue from the OEM group and the control group, with the aim of mapping cellular landscapes, identifying the composition of cell subpopulations, conducting differential gene enrichment analyses, and characterising changes in differentiation trajectories and intercellular communication networks. Key phenotypic findings were further validated through histopathological staining, immunofluorescence, Real-time Reverse Transcription PCR, and Western blot.
Results
A rat model of OEM was successfully established by suturing homologous rat endometrial tissue onto the ovarian surface. Estrous cycle monitoring revealed disrupted estrous cycles in OEM model rats. ELISA demonstrated significantly decreased serum AMH and E2 levels, accompanied by elevated FSH levels in the OEM group. CD10 immunostaining confirmed the positive expression of endometrial tissue, and Prussian blue staining revealed markedly increased iron deposition in the OEM group ovaries. The scRNA-seq identified a total of 70,041 cells, revealing seven major cell types. OEM significantly altered the cellular composition of the ovary, with decreased proportions of granulosa and endothelial cells and an increased overall proportion of immune cells; within the immune-cell compartment, the proportions of macrophages and B cells decreased, whereas those of T cells and neutrophils increased. Granulosa cell analysis revealed disrupted differentiation trajectories, attenuated intercellular AMH and Estradiol signaling, and significantly downregulated mRNA and protein expression of AMH, FSHR, and ESR2 in the OEM group. Stromal cell analysis demonstrated significant enrichment of TGF-β and collagen signaling pathways, with upregulated mRNA and protein expression of COL1A1, TGFB1, and ACTA2 in the OEM group. Masson’s trichrome and Sirius Red staining confirmed significantly increased fibrotic areas in the OEM group ovaries. Immune cell analysis revealed significant enrichment of chemokine signaling and IL-17 signaling pathways, enhanced CCL and CXCL chemokine communication networks, and upregulated mRNA and protein expression of inflammatory mediators, including CXCL1, CCL2, and IL1b in the OEM group.
Conclusions
This study successfully established a rat model that simulates the key pathological features of OEM. Utilizing scRNA-seq, we constructed, for the first time, a comprehensive cellular landscape of the OEM-affected ovary, revealing the synergistic effects of granulosa cell dysfunction, ovarian stromal fibrosis, and immune dysregulation in OEM-induced ovarian functional decline.
Similar content being viewed by others
Acknowledgements
We appreciate every author for their assistance with the experiments and constructive comments on the manuscript.
Funding
This work was supported by the National Natural Science Foundation of China [grant numbers. 82374513], Scientific and technological innovation project of China Academy of Chinese Medical Sciences [grant numbers. CI2021A02402].
Author information
Authors and Affiliations
Corresponding authors
Ethics declarations
Ethics approval and consent to participate
Experimental Animal Ethics Committee of the China Academy of Chinese Medical Sciences approved all the experimental procedures used in this study (Ethics Approval No. IACUC-GAMH-2026-004-01).Not applicable.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Additional information
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Supplementary Information
Rights and permissions
Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
About this article
Cite this article
JIA, Z., HU, G., GUO, Y. et al. A novel rat model of ovarian endometrioma: single-cell RNA sequencing reveals its impact on ovarian function. J Ovarian Res (2026). https://doi.org/10.1186/s13048-026-02313-5
Received:
Accepted:
Published:
DOI: https://doi.org/10.1186/s13048-026-02313-5
Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.
My notes (saved in your browser only)
Ask this paper
Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works
Citation neighborhood (no data yet)
We don't have any in-corpus citations linked to this paper yet. This is a recent paper (2026) — citers typically take a year or two to land, and the OpenAlex reference graph may still be filling in.
Source provenance
- openalex
- last seen: 2026-10-30T06:01:36.263981+00:00
License: CC0
· commercial use OK