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Methylmercury promotes prostacyclin release from cultured human brain microvascular endothelial cells via induction of cyclooxygenase-2 through activation of the EGFR-p38 MAPK pathway by inhibiting protein tyrosine phosphatase 1B activity
http://hdl.handle.net/2241/00150710
http://hdl.handle.net/2241/00150710182a41ad-49c3-4013-81cb-7c9eff2f61d6
名前 / ファイル | ライセンス | アクション |
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Toxicology_392 (1.1 MB)
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Item type | Journal Article(1) | |||||
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公開日 | 2018-02-23 | |||||
タイトル | ||||||
タイトル | Methylmercury promotes prostacyclin release from cultured human brain microvascular endothelial cells via induction of cyclooxygenase-2 through activation of the EGFR-p38 MAPK pathway by inhibiting protein tyrosine phosphatase 1B activity | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源 | http://purl.org/coar/resource_type/c_6501 | |||||
タイプ | journal article | |||||
著者 |
Yoshida, Eiko
× Yoshida, Eiko× Kurita, Masaru× Eto, Komyo× Kumagai, Yoshito× Kaji, Toshiyuki |
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著者別名 |
熊谷, 嘉人
× 熊谷, 嘉人 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Methylmercury is an environmental pollutant that exhibits neurotoxicity when ingested, primarily in the form of neuropathological lesions that localize along deep sulci and fissures, in addition to edematous and inflammatory changes in patient cerebrums. These conditions been known to give rise to a variety of ailments that have come to be collectively termed Minamata disease. Since prostaglandins I2 and E2 (PGI2 and PGE2) increase vascular permeability and contribute to the progression of inflammatory changes, we hypothesize that methylmercury induces the synthesis of these prostaglandins in brain microvascular endothelial cells and pericytes. To test this theory, human brain microvascular endothelial cells and pericytes were cultured and treated with methylmercury, after which the PGI2 and PGE2 released from endothelial cells and/or pericytes were quantified by enzyme-linked immunosorbent assay while protein and mRNA expressions in endothelial cells were analyzed by western blot analysis and real-time reverse transcription polymerase chain reaction, respectively. Experimental results indicate that methylmercury inhibits the activity of protein tyrosine phosphatase 1B, which in turn activates the epidermal growth factor receptor–p38 mitogen-activated protein kinase pathway that induces cyclooxygenase-2 expression. It was also found that the cyclic adenosine 3′,5′-monophosphate pathway, which can be activated by PGI2 and PGE2, is involved in methylmercury-induced cyclooxygenase-2 expression. Since it appears that protein tyrosine phosphatase 1 B serves as a sensor protein for methylmercury in these mechanisms, it is our belief that the results of the present study may provide additional insights into the molecular mechanisms responsible for edematous and inflammatory changes in the cerebrum of patients with Minamata disease. | |||||
書誌情報 |
Toxicology 巻 392, p. 40-46, 発行日 2017-12 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0300-483X | |||||
書誌レコードID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA00864402 | |||||
PubMed番号 | ||||||
識別子タイプ | PMID | |||||
関連識別子 | 28958600 | |||||
DOI | ||||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1016/j.tox.2017.09.013 | |||||
権利 | ||||||
権利情報 | © 2017 The Authors. Published by Elsevier Ireland Ltd. This is an open access article under the CC BY license (http://creativecommons.org/licenses/BY/4.0/). | |||||
著者版フラグ | ||||||
値 | publisher | |||||
出版者 | ||||||
出版者 | Elsevier |