Abstract | BACKGROUND: METHODS: An observational study consisting of 8 cases of women with endometriosis (diagnosed by surgery and histology) and 22 mice of endometriosis animal model was conducted. Granulosa cells were isolated from 16 patients with endometriosis and co-cultured with macrophage under WNT4 treatment using TUNEL assay, quantitative reverse transcription PCR, flow cytometry and ELISA analysis. 22 mice of endometriosis animal model confirmed the WNT4 treatment effects using histology and immunohistochemistry, Western blot and flow cytometry. RESULTS: We observed that the apoptotic proportion of granulosa cells was significantly decreased and M2 macrophage was significantly increased after WNT4 treatment during the granulosa cell and macrophage co-culture system. To reveal the underlying mechanism for this, we conducted a series of experiments and found that high expression of granulosa cell M-CSF led to the M2 polarization of macrophages. The animal model also suggested that the anti-apoptotic effect of WNT4 on granulosa cells were conducted by the M2 polarized macrophage. CONCLUSIONS: WNT4 could reduce granulosa cell apoptosis and improve ovarian reserve by promoting macrophage polarization in endometriosis. M-CSF secreted by granulosa cell after WNT4 treatment was the main mediator of macrophage polarization.
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Authors | Yuan Yuan, Yubin Li, Wen Zhao, Yue Hu, Canquan Zhou, Tengfei Long, Lingli Long |
Journal | Cytokine
(Cytokine)
Vol. 172
Pg. 156400
(12 2023)
ISSN: 1096-0023 [Electronic] England |
PMID | 37839333
(Publication Type: Observational Study, Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2023. Published by Elsevier Ltd. |
Chemical References |
- Macrophage Colony-Stimulating Factor
- Receptors, Estrogen
- Estrogens
- WNT4 protein, human
- Wnt4 Protein
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Topics |
- Humans
- Female
- Mice
- Animals
- Macrophage Colony-Stimulating Factor
(metabolism)
- Endometriosis
(metabolism)
- Receptors, Estrogen
(metabolism)
- Macrophages
(metabolism)
- Granulosa Cells
(metabolism, pathology)
- Apoptosis
- Estrogens
(metabolism)
- Wnt4 Protein
(genetics, metabolism)
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