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https://hdl.handle.net/20.500.14094/E0034028
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2026-08-11
08:41 集計
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40-2_49-63 (fulltext)
pdf
1.59 MB
97
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ファイル出力
メタデータID
E0034028
アクセス権
open access
出版タイプ
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タイトル
ICAM-1 expression and cellular injury in cultured endothelial cells under hypoxia/reoxygenation.
ICAM-1 expression and cellular injury in cultured endothelial cells under hypoxia/reoxygenation.
著者
Mataki, H ; Inagaki, T ; Yokoyama, M ; Maeda, S
著者名
Mataki, H
著者名
Inagaki, T
著者名
Yokoyama, M
著者名
Maeda, S
言語
English (英語)
収録物名
The Kobe journal of the medical sciences
巻(号)
40(2)
ページ
49-63
刊行日
1994
抄録
Intercellular adhesion molecule 1(ICAM-1) expression and cellular changes in human umbilical vein endothelial cells(HUVEC) and ECV304, an established cultured line derived from HUVEC, under hypoxia and hypoxia(H)/reoxygenation(R) were investigated by immunological, cytochemical, and morphological methods. ICAM-1 expression in HUVEC decreased slightly under hypoxia(92%) and was up-regulated under reoxygenation(114%), but this up-regulation was diminished by superoxide dismutase(SOD). The up-regulation of ICAM-1 expression by interleukin-1 beta(IL-1 beta) was detected at almost equal levels under hypoxia, and H/R. Using lucigenin-chemiluminescence, we demonstrated superoxide generation from HUVEC under H/R. The Ca2+ influx under hypoxia, and the Ca2+ release from the cells under H/R reduced by SOD were detected cytochemically. Vacuole formation as cell injury under hypoxia and H/R was detected by electron microscopy. The present findings provide evidence that superoxide generated from HUVEC is responsible for the up-regulation of ICAM-1 expression under H/R, and the cause of endothelial cellular injury.
カテゴリ
The Kobe journal of the medical sciences
>
40巻
>
40巻2号(1994)
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資源タイプ
departmental bulletin paper
ISSN
0023-2513
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NCID
AA00711740
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