Albumin Permeability Across Endothelial Cell Monolayer Exposed to Reactive Oxygen Intermediates : Involvement of Reversible Functional Alteration of the Cell Membrane Ca2+ Channels

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タイトル ( eng )
Albumin Permeability Across Endothelial Cell Monolayer Exposed to Reactive Oxygen Intermediates : Involvement of Reversible Functional Alteration of the Cell Membrane Ca2+ Channels
作成者
Az-Ma Toshiharu
Fujii Kohyu
Yuge Osafumi
収録物名
Hiroshima Journal of Medical Sciences
49
1
開始ページ 57
終了ページ 65
収録物識別子
[PISSN] 0018-2052
[EISSN] 2433-7668
[NCID] AA00664312
抄録
This study was designed to test the idea that the redox state of sulfhydryl (SH)-groups in cell-membrane Ca2+ channels plays a pivotal role in Ca2+ influx, which in turn causes an increase in albumin permeability across the cultured monolayer of porcine pulmonary artery endothelial (PPAE) cells exposed to xanthine/xanthine oxidase (X/XO). Albumin permeability as well as the concentration of intracellular Ca2+ ([Ca2+]i) was increased by X/XO. A H202 scavenger (catalase), an iron chelator (o-phenanthroline), and a hydroxyl radical scavenger (dimethyl sulfoxide) inhibited these changes provoked by X/XO, in which intracellular iron-catalyzed hydroxyl radical generation was suggested to be involved. The increase in albumin permeability and [Ca2+]i continued once the PPAE cells were exposed to X/XO. The [Ca2+]i was decreased by a Ca2+ channel blocker, Ni2+, while the removal of Ni2+ increased [Ca2+]i again, suggesting the sustained Ca2+ influx through cell-membrane Ca2+ channels was responsible for the [Ca2+]i elevation. Ni2+ failed to inhibit albumin permeability sustained after the removal of X/XO. In contrast, SH-reducing agents (dithiothreitol and glutathione) inhibited the sustained permeability as well as Ca2+ influx. We concluded that the redox alteration of SH-groups in cell-membrane Ca2+ channels was involved in the increase in albumin permeability after exposure of the endothelial cells to oxidative stress.
著者キーワード
Albumin permeability
Reactive oxygen intermediates
Calcium channels
Redox state
内容記述
This study was supported in part by a Grant-in-aid for Scientific Research from the Ministry of Education, Science and Culture of Japan (No. 09771160).
NDC分類
医学 [ 490 ]
言語
英語
資源タイプ 紀要論文
出版者
Hiroshima University Medical Press
発行日 2000-03
出版タイプ Version of Record(出版社版。早期公開を含む)
アクセス権 オープンアクセス
収録物識別子
[ISSN] 0018-2052
[NCID] AA00664312