Macrophages Protect Endometriotic Cells Against Oxidative Damage Through a Cross-Talk Mechanism.

• Material Type: 博士論文
• Title: Macrophages Protect Endometriotic Cells Against Oxidative Damage Through a Cross-Talk Mechanism.
• Author/Editor: Ogawa, Kenji; Liu, Tingting; Kawahara, Naoki; Kobayashi, Hiroshi
• Author Heading: Ogawa, Kenji; Liu, Tingting; Kawahara, Naoki; Kobayashi, Hiroshi
• Publication, Distribution, etc.: Springer Nature
• Publication Date: 2022-08
• Publication Date (W3CDTF): 2022-08
• Alternative Title: マクロファージはクロストーク機構により子宮内膜細胞を酸化ストレスから保護する
• Periodical title: Reproductive sciences
• No. or year of volume/issue: 29 8
• Volume: 29
• Issue: 8
• Pages: 2165-2178
• ISSN (Periodical Title): ISSN : 1933-7191
• Degree grantor/type: 奈良県立医科大学
• Date Granted: 2022-09-28
• Dissertation Number: 甲第849号
• Degree Type: 博士（医学）
• Text Language Code: eng
• Subject Heading: Co-culture; Endometriosis; Heme oxygenase-1; Macrophages, Transforming growth factor-beta
• Target Audience: 一般
• Note (General): type:Thesis; This aim of this study was to investigate whether macrophages protect endometriotic cells from oxidative injury and to elucidate the underlying mechanisms of any protection. Endometriotic cells cultured with or without differentiated macrophages (dTHP-1 cells) were treated with hydrogen peroxide (H2O2) or methemoglobin, a major component of hemoglobin species in endometriotic cyst fluid. Co-culture experiments, microarray analysis, screening and validation of differentially expressed genes (DEGs), cell proliferation and viability assays, and experiments using a specific inhibitor were conducted to investigate the functional cross-talk between endometriotic cells and macrophages. Microarray analysis revealed that endometriotic cells co-cultured with dTHP-1 differentially express several genes compared with monoculture. Quantitative enzyme-linked immunosorbent assay (ELISA) and Western blotting analysis identified TGF-β1 as a promising candidate gene expressed in endometriotic cells co-cultured with dTHP-1 cells. TGF-β1 stimulated the expression of heme oxygenase-1 (HO-1) in dTHP-1 cells. HO-1 expression was increased in dTHP-1 cells co-cultured with endometriotic cells compared with the dTHP-1 monoculture. Both H2O2 and methemoglobin upregulated the expression of the HO-1 protein in the dTHP-1 monoculture; moreover, co-culture with endometriotic cells further enhanced HO-1 production. The co-culture with dTHP-1 protected endometriotic cells against oxidative injury. Blockade of HO-1 abolished the protective effects of macrophages. In an oxidative stress environment, TGF-β1 produced by endometriotic cells may protect against oxidative injury through the upregulation of macrophage-derived HO-1. The cross-talk between endometriotic cells and macrophages may contribute to the progression and pathogenesis of endometriosis.; 博士（医学）・甲第849号・令和4年9月28日; Copyright © 2022, Society for Reproductive Investigation.; © 2022 Springer Nature Switzerland AG.; The version of record of this article, first published in Reproductive Sciences, is available online at Publisher's website: https://doi.org/10.1007/s43032-022-00890-6.; identifier:Reproductive sciences Vol.29 No.8 p.2165-2178 (2022 Aug); identifier:19337191; identifier:http://ginmu.naramed-u.ac.jp/dspace/handle/10564/4076; identifier:Reproductive sciences, 29(8): 2165-2178
• Access Restrictions: インターネット公開
• Related Material (DOI): 10.1007/s43032-022-00890-6
• Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）; https://irdb.nii.ac.jp
• Original Data Provider (Database): 奈良県立医科大学 : 奈良県立医科大学機関リポジトリ GINMU

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http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/4076/1/01%e7%94%b2849%e6%9c%ac%e6%96%87%e3%81%ae%e8%a6%81%e6%97%a8.pdf fulltext

http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/4076/2/02%e7%94%b2849%e5%af%a9%e6%9f%bb%e8%a6%81%e6%97%a8.pdf fulltext

http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/4076/6/03%e7%94%b2849%e6%9c%ac%e6%96%87.pdf fulltext

http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/4076/7/04%e7%94%b2849%e6%9c%ac%e6%96%87%28Fig.1%2c2%2c3%2c4A%2c4B%2c5A%2c5B%2c6%2c7%29.pdf fulltext