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著作: [日吉 峰麗]/Indalao I.L/[矢野 仁康]/[山根 一彦]/[高橋 悦久]/[木戸 博]/Influenza A virus infection of vascular endothelial cells induces GSK-3β-mediated β-catenin degradation in adherens junctions, with a resultant increase in membrane permeability./[Archives of Virology]

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EID
289503
EOID
816364
Map
0
LastModified
2016年4月19日(火) 19:16:28
Operator
大家 隆弘
Avail
TRUE
Censor
0
Owner
高橋 悦久
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種別 必須 学術論文(審査論文)
言語 必須 英語
招待 推奨
審査 推奨
カテゴリ 推奨
共著種別 推奨
学究種別 推奨
組織 推奨
著者 必須
  1. 日吉 峰麗
    役割 任意
    貢献度 任意
    学籍番号 推奨
  2. (英) Indalao I.L
    役割 任意
    貢献度 任意
    学籍番号 推奨
  3. 矢野 仁康
    役割 任意
    貢献度 任意
    学籍番号 推奨
  4. 山根 一彦
    役割 任意
    貢献度 任意
    学籍番号 推奨
  5. 高橋 悦久([徳島大学.先端酵素学研究所.重点研究部門])
    役割 任意
    貢献度 任意
    学籍番号 推奨
  6. 木戸 博([徳島大学.先端酵素学研究所.重点研究部門])
    役割 任意
    貢献度 任意
    学籍番号 推奨
題名 必須

(英) Influenza A virus infection of vascular endothelial cells induces GSK-3β-mediated β-catenin degradation in adherens junctions, with a resultant increase in membrane permeability.

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要約 任意

(英) Multiorgan failure with vascular hyperpermeability is the final outcome in the progression of seasonal influenza virus pneumonia and influenza-associated encephalopathy, and it is also common in infection with highly pathogenic avian influenza virus. However, the precise molecular mechanism by which influenza virus infection causes vascular endothelial cell hyperpermeability remains poorly defined. We investigated the mechanisms of hyperpermeability of human umbilical vein endothelial cells infected with influenza A virus (IAV)/Puerto Rico/8/34 (PR8) (H1N1). The levels of β-catenin, a key regulatory component of the vascular endothelial-cadherin cell adhesion complex, were markedly decreased during infection for 28 h, with increments of vascular hyperpermeability measured by transendothelial electrical resistance. Lactacystin (at 2 μM), a proteasome inhibitor, inhibited the decrease in β-catenin levels. Since the N-terminal phosphorylation of β-catenin by glycogen synthase kinase (GSK)-3β is the initiation step of proteasome-dependent degradation, we examined the effects of GSK-3β suppression by RNA interference in endothelial cells. IAV-infection-induced β-catenin degradation was significantly inhibited in GSK-3β-knockdown cells, and transfection of cells with recombinant β-catenin significantly suppressed IAV-induced hyperpermeability. These findings suggest that IAV infection induces GSK-3β-mediated β-catenin degradation in the adherens junctional complexes and induces vascular hyperpermeability. The in vitro findings of β-catenin degradation and activation of GSK-3β after IAV infection were confirmed in lungs of mice infected with IAV PR8 during the course of infection from day 0 to day 6. These results suggest that GSK-3β-mediated β-catenin degradation in adherens junctions is one of the key mechanisms of vascular hyperpermeability in severe influenza.

キーワード 推奨
  1. (英) Adherens Junctions
  2. (英) Animals
  3. (英) Cell Membrane
  4. (英) Cells, Cultured
  5. (英) Endothelial Cells
  6. (英) Female
  7. (英) Gene Silencing
  8. (英) Glycogen Synthase Kinase 3
  9. (英) Humans
  10. (英) Influenza A Virus, H1N1 Subtype
  11. (英) Mice
  12. (英) Mice, Inbred C57BL
  13. (英) Permeability
  14. (英) beta Catenin
発行所 推奨
誌名 必須 Archives of Virology(International Union of Microbiological Societies)
(pISSN: 0304-8608, eISSN: 1432-8798)
ISSN 任意 1432-8798
ISSN: 0304-8608 (pISSN: 0304-8608, eISSN: 1432-8798)
Title: Archives of virology
Title(ISO): Arch Virol
Supplier: Springer Online Journal Archive
Publisher: Springer Wien
 (NLM Catalog  (Scopus  (CrossRef (Scopus information is found. [need login])
必須 160
必須 1
必須 225 234
都市 任意
年月日 必須 2014年 11月 12日
URL 任意
DOI 任意 10.1007/s00705-014-2270-5    (→Scopusで検索)
PMID 任意 25385175    (→Scopusで検索)
NAID 任意
WOS 任意
Scopus 任意
評価値 任意
被引用数 任意
指導教員 推奨
備考 任意
  1. (英) Article.ELocationID: 10.1007/s00705-014-2270-5

  2. (英) Article.PublicationTypeList.PublicationType: Journal Article

  3. (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't

  4. (英) OtherID: PMC4284391