論文 - 詳細
RRC ID | 70168 |
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著者 | Yamashita S, Hashimoto K, Sawada I, Ogawa M, Nakatsuka E, Kawano M, Kinose Y, Kodama M, Sawada K, Kimura T. |
タイトル | Endometrial galectin-3 causes endometriosis by supporting eutopic endometrial cell survival and engraftment in the peritoneal cavity. |
ジャーナル | Am J Reprod Immunol |
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. |
巻・号 | 87(6) |
ページ | e13533 |
公開日 | 2022-6-1 |
DOI | 10.1111/aji.13533 |
PMID | 35366371 |
MeSH | Antigens, Neoplasm Biomarkers, Tumor Cell Survival Endometriosis* Endometrium / pathology Female Galectin 3 / genetics Galectin 3 / metabolism Humans Peritoneal Cavity / pathology Proteomics Stromal Cells / metabolism |
IF | 2.739 |
リソース情報 | |
ヒト・動物細胞 | 293gp(RCB2354) |