Uterine-derived exosomes induce the M2 polarization of macrophages via miR210-3p to promote the development of endometriosis

Shengnan Chen, Ying Jiang, Xiaoshan Chai, Zhaoying Chen, Hao Tian, Min Liu, Tianyu Zhu, Wanwan ShangGuan, Xianqing Wu
In: Research Square · 2023 · doi:10.21203/rs.3.rs-3030329/v1 · W4379979379
preprint OA: green CC0
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Uterine-derived exosomes from endometriosis patients upregulate miR-210-3p in peritoneal macrophages, inducing M2 polarization and promoting lesion development by inhibiting ATP5D.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-09 ⓘ

This preprint investigates whether uterine-derived exosomes from patients with endometriosis can modulate peritoneal macrophages to influence endometriosis development. Using macrophage conditioned media and uterine exosomes from endometriosis versus control groups, the study reports that endometriosis-associated exosomes increased miR-210-3p expression in peritoneal macrophages, induced M2 polarization, and promoted macrophage-associated tumorigenic behaviors including proliferation, invasion, and progesterone resistance in cellular assays, with in vivo confirmation in a C57BL/6 mouse endometriosis model where miR-210-3p inhibition reduced ectopic lesion number and volume. Mechanistically, miR-210-3p was described as driving M2 polarization by inhibiting ATP5D expression. The paper notes a key caveat that it is a preprint not yet peer reviewed. This paper is centrally about endometriosis — it tests uterine-derived exosomes and miR-210-3p–mediated M2 macrophage polarization as a mechanism promoting endometriosis progression.

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Abstract

Abstract Background Endometriosis development is associated with peritoneal immune microenvironment abnormality. However, the specific mechanism is uncertain. Investigating peritoneal immune microenvironment regulation mechanisms could introduce novel therapeutic strategies for effective endometriosis treatment. Methods Wound healing assay, Transwell, colony formation were carried out to assess cells invasion and proliferation. Western blotting analysis and ELISA were used to evaluate cells resistance to progesterone. Endometriosis C57BL6 mouse model was conducted to assess the impact of peritoneal inflammatory environment and macrophage miR-210-3p on ectopic lesion implantation and growth. miRNA and proteomics sequencing were carried out to verify the potential mechanisms influencing the development of endometriosis. Results Medium conditioned of peritoneal macrophages from patients with endometriosis, as well as the medium conditioned of macrophages treated with uterine-derived exosomes of endometriosis patients, promoted the proliferation, invasion and progesterone resistance of cells. Interestingly, Uterine-derived exosomes of endometriosis patients increased miR-210-3p expression in peritoneal macrophages. In vivo experiments confirmed that macrophages lentivirally transduced with miR-210-3p inhibitor can significantly decrease the number and volume of endometriotic lesions. Mechanistically, miR-210-3p significantly induced M2 macrophage polarization by inhibiting the expression of ATP5D, and promoted cells migration. Conclusions Uterine-derived exosomes of endometriosis patients upregulated the expression of miR-210-3p in peritoneal macrophages to inhibit ATP5D, driving macrophages polarization towards M2 and promoting the development of endometriosis.

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endometriosis

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