Endometriosis disrupts oocyte metabolism and cortical granule function, impairing fertilization

Omar G. Klinsky, Klinsky OG, Paula A Wetten, Wetten PA, Julio E Romani, Romani JE, Abraham EC, Emilia C Abraham, Michaut MA, Marcela A. Michaut
Reproductive biology and endocrinology : RB&E · 2026 · vol. 24(1) · doi:10.1186/s12958-026-01571-8 · PMID:42186024 · PMC13386785 · W7162328098
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Endometriosis disrupts oocyte metabolism and cortical granule exocytosis due to altered actin and reduced SNARE regulators, impairing fertilization while maintaining early embryonic activation.

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⚙ AI-generated deep summary by claude@2026-07, 2026-07-14 · read from full text ⓘ

This paper studied whether experimentally induced endometriosis in an autologous surgically induced mouse model disrupts oocyte cytoplasmic maturation, assessing oocyte metabolism, cortical granule biology and exocytosis, actin architecture, SNARE-regulated membrane fusion machinery, fertilization outcome, and early embryonic activation. The authors found that endometriosis increased intracellular reactive oxygen species and altered acidic vesicular compartments, while cortical granule localization was preserved but strontium chloride–induced cortical granule exocytosis failed to occur. These defects were associated with a thickened cortical F-actin cytoskeleton and reduced levels of α-SNAP and NSF, and endometriotic oocytes showed decreased fertilization rates without evidence of polyspermy, whereas TPEN-induced parthenogenetic activation and second polar body extrusion were unchanged. The paper’s limitation is that it uses a mouse model of endometriosis, which may not fully capture human disease context. This paper is centrally about endometriosis—specifically endometriosis-associated impairments in oocyte metabolism, cortical granule exocytosis, and SNARE/actin-related fertilization competence.

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Abstract

BACKGROUND: Endometriosis is a chronic inflammatory disease strongly associated with reduced oocyte quality and subfertility, yet the underlying cytoplasmic defects remain poorly understood. METHODS: Using a surgically induced autologous mouse model, we examined whether endometriosis alters oocyte metabolism, cortical granule (CG) biology, actin architecture, SNARE-regulated exocytosis, fertilization, and early embryonic activation. RESULTS: Endometriosis markedly increased intracellular reactive oxygen species and altered quinacrine-positive acidic vesicular compartments in ovulated oocytes. Although CG localization was preserved, endometriotic oocytes failed to undergo strontium chloride-induced CG exocytosis. These defects correlated with a significantly thickened cortical F-actin cytoskeleton and a substantial reduction in α-SNAP and NSF levels-two essential regulators of SNARE complex disassembly and membrane fusion. Functionally, endometriotic oocytes exhibited decreased fertilization rates without evidence of polyspermy, while their ability to undergo TPEN-induced parthenogenetic activation and second polar body extrusion remained unchanged. CONCLUSIONS: These findings demonstrate that endometriosis impairs multiple aspects of cytoplasmic maturation-metabolic homeostasis, actin remodeling, and CG exocytotic machinery-ultimately reducing sperm-oocyte fusion efficiency while preserving early embryonic activation capacity. This mechanistic insight provides a foundation for understanding how endometriosis compromises oocyte competence.
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Abstract

Background Endometriosis is a chronic inflammatory disease strongly associated with reduced oocyte quality and subfertility, yet the underlying cytoplasmic defects remain poorly understood.

Methods

Using a surgically induced autologous mouse model, we examined whether endometriosis alters oocyte metabolism, cortical granule (CG) biology, actin architecture, SNARE-regulated exocytosis, fertilization, and early embryonic activation.

Results

Endometriosis markedly increased intracellular reactive oxygen species and altered quinacrine-positive acidic vesicular compartments in ovulated oocytes. Although CG localization was preserved, endometriotic oocytes failed to undergo strontium chloride–induced CG exocytosis. These defects correlated with a significantly thickened cortical F-actin cytoskeleton and a substantial reduction in α-SNAP and NSF levels—two essential regulators of SNARE complex disassembly and membrane fusion. Functionally, endometriotic oocytes exhibited decreased fertilization rates without evidence of polyspermy, while their ability to undergo TPEN-induced parthenogenetic activation and second polar body extrusion remained unchanged.

Conclusions

These findings demonstrate that endometriosis impairs multiple aspects of cytoplasmic maturation—metabolic homeostasis, actin remodeling, and CG exocytotic machinery—ultimately reducing sperm–oocyte fusion efficiency while preserving early embryonic activation capacity. This mechanistic insight provides a foundation for understanding how endometriosis compromises oocyte competence. Similar content being viewed by others Abbreviations - α-SNAP: - Alpha-soluble NSF attachment protein - BS: - Blocking solution - BSA: - Bovine serum albumin - CCCP: - Carbonyl cyanide 3-chlorophenylhydrazone - CG: - Cortical granule - CGE: - Cortical granule exocytosis - COCs: - Cumulus–oocyte complexes - DCF-DA: - Dichlorofluorescin diacetate - DPBS: - Dulbecco’s phosphate-buffered saline - Endo: - Endometriosis group - F-actin: - Filamentous actin - GV: - Germinal vesicle - hCG: - Human chorionic gonadotropin - HTF: - Human Tubal Fluid medium - i.p.: - Intraperitoneally - IVF: - In vitro fertilization - LCA-FITC: - Lens Culinaris Agglutinin labeled with Fluorescein Isothiocyanate - MII: - Metaphase II - MMP: - Mitochondrial membrane potential - NSF: - N-ethylmaleimide-sensitive factor - PBS: - Phosphate-buffered saline - PFA: - Paraformaldehyde - PMSG: - Purified equine chorionic gonadotropin - PVA: - Polyvinyl alcohol - ROS: - Reactive oxygen species - RT: - Room temperature - SEM: - Standard Error of the Mean - SNARE: - Soluble N-ethylmaleimide-sensitive factor Attachment protein Receptor - SrCl2: - Strontium chloride - TMRE: - t-ditetramethyl rhodamine methyl ester - TPEN: - N,N,N′,N′-Tetrakis (2-pyridylmethyl) ethylenediamine

Acknowledgements

The authors are very grateful to Dr. Marilina Casais (Instituto Multidisciplinario de Investigaciones Biológicas de San Luis, Universidad Nacional de San Luis-CONICET, San Luis, Argentina) for her instruction in the development of the endometriosis model used in this work. The authors acknowledge the help of Veterinarian Julieta Scelta in the maintenance of the animal facility and Engr. Elisa Bocanegra and Dr. Jorge Ibáñez for excellent technical assistance (IHEM, UNCUYO-CONICET, Mendoza, Argentina). OGK, PAW and ECA are thankful to CONICET, Argentina, for fellowships. JER is thankful to Agencia I+D+i, Argentina, for his fellowship. Funding This work was funded by Agencia Nacional de Promoción Científica y Tecnológica (grant PICT 2020–03627 to MAM), Argentina, and Universidad Nacional de Cuyo (grants 06/M025-T1, J050-T1, PIO 80020230100017 N, and 06/80020240400085UN to MAM; 80020240200084UN to ECA), Mendoza, Argentina. Author information Authors and Affiliations Corresponding author Ethics declarations Ethics approval and consent to participate All experimental procedures were performed in accordance with the Guiding Principles in the Care and Use of Animals of the US National Institutes of Health. Protocols were approved by the Institutional Animal Care and Use Committee of the School of Medical Science, Universidad Nacional de Cuyo (Protocol No. 227/2022). 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-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, 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 you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. 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-nc-nd/4.0/. About this article Cite this article Klinsky, O.G., Wetten, P.A., Romani, J.E. et al. Endometriosis disrupts oocyte metabolism and cortical granule function, impairing fertilization. Reprod Biol Endocrinol (2026). https://doi.org/10.1186/s12958-026-01571-8 Received: Accepted: Published: DOI: https://doi.org/10.1186/s12958-026-01571-8

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Condition tags

endometriosis

MeSH descriptors

Cytoplasmic Granules Cytoplasmic Granules Cytoplasmic Granules Cytoplasmic Granules Cytoplasmic Granules Cytoplasmic Granules Cytoplasmic Granules Cytoplasmic Granules Cytoplasmic Granules Cytoplasmic Granules Cytoplasmic Granules Cytoplasmic Granules Cytoplasmic Granules Cytoplasmic Granules Cytoplasmic Granules Cytoplasmic Granules Cytoplasmic Granules Cytoplasmic Granules Cytoplasmic Granules Cytoplasmic Granules

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References (51)

SciLite annotations

organisms 1
transgenic mice
chemicals 3
oxygen quinacrine chloride

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