Endometrial galectin‐3 causes endometriosis by supporting eutopic endometrial cell survival and engraftment in the peritoneal cavity

Yamashita S, Saya Yamashita, Kae Hashimoto, Ikuko Sawada, Sawada I, Minori Ogawa, Ogawa M, Erika Nakatsuka, Nakatsuka E, Mahiru Kawano, Kawano M, Yasuto Kinose, Kinose Y, Michiko Kodama, Kodama M, Sawada K, Kenjiro Sawada, Tadashi Kimura, Kimura T
American journal of reproductive immunology (New York, N.Y. : 1989) · 2022 · vol. 87(6) , pp. e13533 · doi:10.1111/aji.13533 · PMID:35366371 · W4224121127
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Galectin-3, overexpressed in the eutopic endometrium of endometriosis patients, enhances endometrial stromal cell adhesion, migration, and survival by reducing natural killer cell cytotoxicity.

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Abstract

PROBLEM: The pathogenesis of endometriosis remains unclear. Endometrial cells in retrograde menstruation are considered the source of endometriosis; therefore, we hypothesized that the eutopic endometrium may provide clues regarding the pathogenesis. We aimed to clarify the role of eutopic endometrial cells in endometriosis development. METHOD OF STUDY: Eutopic endometrial tissues were obtained from patients with or without endometriosis, and expression of cell surface molecules in eutopic endometrial stromal cells (ESCs) was evaluated via iTRAQ-based proteomic analysis. Based on the results, we focused on galectin-3. Galectin-3 expression in clinical samples was confirmed by immunohistochemistry and Western blot analysis. The concentration of secreted galectin-3 was measured using enzyme-linked immunosorbent assays. Adhesion and migration of ESCs were evaluated by in vitro adhesion and wound healing assays. The cytotoxicity of natural killer cells was measured via calcein release assays. Cell proliferation was measured using the CyQUANT Cell Proliferation Assay Kit. RESULTS: iTRAQ analysis revealed that galectin-3 expression was specifically elevated in the ESCs from endometriosis patients. Immunohistochemistry confirmed galectin-3 overexpression in the eutopic endometrium of endometriosis, irrespective of the menstrual phase. Galectin-3 was overexpressed and secreted by the eutopic ESCs from patients with endometriosis compared to that from patients without endometriosis. Galectin-3 expression in ESCs increased adhesion and migration, whereas galectin-3 inhibitors impaired these processes. Galectin-3 reduced the cytotoxicity of natural killer cells toward ESCs, while not affecting cell proliferation. CONCLUSION: Galectin-3 promotes peritoneal engraftment of ESCs due to impaired immune surveillance in the peritoneal cavity and increases ESCs adhesion and migration to the peritoneum.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Antigens, Neoplasm Antigens, Neoplasm Antigens, Neoplasm Antigens, Neoplasm Biomarkers, Tumor Biomarkers, Tumor Biomarkers, Tumor Biomarkers, Tumor Cell Survival Cell Survival Cell Survival Cell Survival Endometrium Endometrium Endometrium Endometrium

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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. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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Cited by (6)

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