MARCKS is involved in methylmercury-induced decrease in cell viability and nitric oxide production in EA.hy926 cells

• VAN DAO Cuong

  Department of Veterinary Pharmacology, Joint Faculty of Veterinary Medicine, Kagoshima University, 1–21–24 Korimoto, Kagoshima 890–0065, Japan Department of Veterinary Pharmacology, Faculty of Animal Husbandry and Veterinary Medicine, Thai Nguyen University of Agriculture and Forestry, Group 10, Quyet Thang Commune, Thai Nguyen City, Thai Nguyen, Vietnam

• ISLAM Md. Zahorul

  Department of Veterinary Pharmacology, Joint Faculty of Veterinary Medicine, Kagoshima University, 1–21–24 Korimoto, Kagoshima 890–0065, Japan

• SUDO Kasumi

  Department of Veterinary Pharmacology, Joint Faculty of Veterinary Medicine, Kagoshima University, 1–21–24 Korimoto, Kagoshima 890–0065, Japan

• SHIRAISHI Mitsuya

  Department of Veterinary Pharmacology, Joint Faculty of Veterinary Medicine, Kagoshima University, 1–21–24 Korimoto, Kagoshima 890–0065, Japan

• MIYAMOTO Atsushi

  Department of Veterinary Pharmacology, Joint Faculty of Veterinary Medicine, Kagoshima University, 1–21–24 Korimoto, Kagoshima 890–0065, Japan

抄録

Methylmercury (MeHg) is a persistent environmental contaminant that has been reported worldwide. MeHg exposure has been reported to lead to increased risk of cardiovascular diseases; however, the mechanisms underlying the toxic effects of MeHg on the cardiovascular system have not been well elucidated. We have previously reported that mice exposed to MeHg had increased blood pressure along with impaired endothelium-dependent vasodilation. In this study, we investigated the toxic effects of MeHg on a human endothelial cell line, EA.hy926. In addition, we have tried to elucidate the role of myristoylated alanine-rich C kinase substrate (MARCKS) in the MeHg toxicity mechanism in EA.hy926 cells. Cells exposed to MeHg (0.1–10 µM) for 24 hr showed decreased cell viability in a dose-dependent manner. Treatment with submaximal concentrations of MeHg decreased cell migration in the wound healing assay, tube formation on Matrigel and spontaneous nitric oxide (NO) production of EA.hy926 cells. MeHg exposure also elicited a decrease in MARCKS expression and an increase in MARCKS phosphorylation. MARCKS knockdown or MARCKS overexpression in EA.hy926 cells altered not only cell functions, such as migration, tube formation and NO production, but also MeHg-induced decrease in cell viability and NO production. These results suggest the broad role played by MARCKS in endothelial cell functions and the involvement of MARCKS in MeHg-induced toxicity.

収録刊行物

• Ｔｈｅ　Ｊｏｕｒｎａｌ　ｏｆ　Ｖｅｔｅｒｉｎａｒｙ　Ｍｅｄｉｃａｌ　Ｓｃｉｅｎｃｅ

  Ｔｈｅ　Ｊｏｕｒｎａｌ　ｏｆ　Ｖｅｔｅｒｉｎａｒｙ　Ｍｅｄｉｃａｌ　Ｓｃｉｅｎｃｅ 78 (10), 1569-1576, 2016

  公益社団法人 日本獣医学会

キーワード

• EA.hy926 cells
• endothelium
• MARCKS
• methylmercury
• nitric oxide

詳細情報

• CRID: 1390282681407748992
• NII論文ID: 130005267951
• NII書誌ID: AA10796138
• DOI: 10.1292/jvms.16-0249
• ISSN: 13477439
• ISSN: 09167250
• NDL書誌ID: 027729906
• PubMed: 27349763
• Web Site: http://id.ndl.go.jp/bib/027729906
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I027729906
• Web Site: https://www.jstage.jst.go.jp/article/jvms/78/10/78_16-0249/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2017175377
• 本文言語コード: en
• データソース種別:
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  • NDL
  • Crossref
  • PubMed
  • CiNii Articles
  • KAKEN
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