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METHODS: TLR4 expression was examined in macrophages (Mφ) isolated in primary culture from the peritoneal fluid of women with and without endometriosis. The production of a number of macromolecules by non-treated Mφ, Hsp70-treated Mφ and after treatment with anti-TLR4 antibody was examined by enzyme linked immunosorbent assay (ELISA). The single and combined effects of Hsp70 and lipopolysaccharide (LPS) on the growth of endometrial stromal cells were analyzed by 5-bromo-2-deoxyuridine (BrdU) incorporation study. Hsp70 levels in eutopic and ectopic endometria were measured by ELISA. RESULTS: TLR4 was detected in isolated Mφ at protein and gene level. Hsp70 (10 μg/ml) significantly stimulated the production of hepatocyte growth factor, vascular endothelial cell growth factor, interleukin-6 and tumor necrosis factor alpha by Mφ derived from women with endometriosis compared with Mφ derived from women with no endometriosis (P \u003c 0.05 for each). This effect of Hsp70 was abrogated after pretreatment of Mφ with anti-TLR4 antibody. BrdU incorporation indicated that Hsp70 significantly enhanced the growth of endometrial stromal cells (?50% increase) from women with endometriosis compared to non-treated cells. A synergistic effect on cell proliferation was observed between exogenous Hsp70 and LPS and this was significantly suppressed by pretreatment of cells with anti-TLR4 antibody (P \u003c 0.05). Tissue levels of Hsp70 were significantly higher in the eutopic endometria (P \u003c 0.05) and opaque red lesions (P \u003c 0.01) derived from women with endometriosis than from other peritoneal lesions or from women with no endometriosis. CONCLUSIONS: A prominent stress reaction was observed in blood-filled opaque red peritoneal lesions. 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Toll-like receptor 4-mediated growth of endometriosis by human heat-shock protein 70
http://hdl.handle.net/10069/22227
http://hdl.handle.net/10069/22227c0f6333a-288e-460b-9bbc-bf97b8d1220c
名前 / ファイル | ライセンス | アクション |
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HumRep23_2210.pdf (96.2 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2009-10-08 | |||||
タイトル | ||||||
タイトル | Toll-like receptor 4-mediated growth of endometriosis by human heat-shock protein 70 | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Cell growth | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Endometriosis | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Hsp70 | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | LPS | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Macrophages | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | TLR4 | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
Khan, Khaleque Newaz
× Khan, Khaleque Newaz× Kitajima, Michio× Imamura, Takehito× Hiraki, Koichi× Fujishita, Akira× Sekine, Ichiro× Ishimaru, T× Masuzaki, Hideaki |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | BACKGROUND: We investigated the role of human heat-shock protein 70 (Hsp70) in Toll-like receptor 4 (TLR4)-mediated growth of endometriosis. METHODS: TLR4 expression was examined in macrophages (Mφ) isolated in primary culture from the peritoneal fluid of women with and without endometriosis. The production of a number of macromolecules by non-treated Mφ, Hsp70-treated Mφ and after treatment with anti-TLR4 antibody was examined by enzyme linked immunosorbent assay (ELISA). The single and combined effects of Hsp70 and lipopolysaccharide (LPS) on the growth of endometrial stromal cells were analyzed by 5-bromo-2-deoxyuridine (BrdU) incorporation study. Hsp70 levels in eutopic and ectopic endometria were measured by ELISA. RESULTS: TLR4 was detected in isolated Mφ at protein and gene level. Hsp70 (10 μg/ml) significantly stimulated the production of hepatocyte growth factor, vascular endothelial cell growth factor, interleukin-6 and tumor necrosis factor alpha by Mφ derived from women with endometriosis compared with Mφ derived from women with no endometriosis (P < 0.05 for each). This effect of Hsp70 was abrogated after pretreatment of Mφ with anti-TLR4 antibody. BrdU incorporation indicated that Hsp70 significantly enhanced the growth of endometrial stromal cells (?50% increase) from women with endometriosis compared to non-treated cells. A synergistic effect on cell proliferation was observed between exogenous Hsp70 and LPS and this was significantly suppressed by pretreatment of cells with anti-TLR4 antibody (P < 0.05). Tissue levels of Hsp70 were significantly higher in the eutopic endometria (P < 0.05) and opaque red lesions (P < 0.01) derived from women with endometriosis than from other peritoneal lesions or from women with no endometriosis. CONCLUSIONS: A prominent stress reaction was observed in blood-filled opaque red peritoneal lesions. Human Hsp70 induces pelvic inflammation and may be involved in TLR4-mediated growth of endometrial cells derived from women with endometriosis. | |||||
内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | without figures and tables | |||||
書誌情報 |
Human Reproduction 巻 23, 号 10, p. 2210-2219, 発行日 2008-10 |
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出版者 | ||||||
出版者 | Oxford University Press | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 02681161 | |||||
EISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 1460-2350 | |||||
書誌レコードID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA10691537 | |||||
DOI | ||||||
関連タイプ | isVersionOf | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1093/humrep/den195 | |||||
権利 | ||||||
権利情報 | c The Author 2008. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. | |||||
権利 | ||||||
権利情報 | This is a pre-copy-editing, author-produced PDF of an article accepted for publication in Human Reproduction following peer review. The definitive publisher-authenticated version Human Reproduction, 23(10), pp.2210-2219; 2008 is available online at: http://humrep.oxfordjournals.org/cgi/content/abstract/23/10/2210 . | |||||
著者版フラグ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | Human Reproduction, 23(10), pp.2210-2219; 2008 |