Item type |
デフォルトアイテムタイプ_(フル)(1) |
公開日 |
2023-03-18 |
タイトル |
|
|
タイトル |
Albumin Permeability Across Endothelial Cell Monolayer Exposed to Reactive Oxygen Intermediates : Involvement of Reversible Functional Alteration of the Cell Membrane Ca2+ Channels |
|
言語 |
en |
作成者 |
Saeki, Noboru
Az-Ma, Toshiharu
Fujii, Kohyu
Kawamoto, Masashi
Yuge, Osafumi
|
アクセス権 |
|
|
アクセス権 |
open access |
|
アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
主題 |
|
|
主題Scheme |
Other |
|
主題 |
Albumin permeability |
主題 |
|
|
主題Scheme |
Other |
|
主題 |
Reactive oxygen intermediates |
主題 |
|
|
主題Scheme |
Other |
|
主題 |
Calcium channels |
主題 |
|
|
主題Scheme |
Other |
|
主題 |
Redox state |
主題 |
|
|
主題Scheme |
NDC |
|
主題 |
490 |
内容記述 |
|
|
内容記述 |
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. |
|
言語 |
en |
内容記述 |
|
|
内容記述タイプ |
Other |
|
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). |
出版者 |
|
|
出版者 |
Hiroshima University Medical Press |
言語 |
|
|
言語 |
eng |
資源タイプ |
|
|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
departmental bulletin paper |
出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
収録物識別子 |
|
|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
0018-2052 |
収録物識別子 |
|
|
収録物識別子タイプ |
NCID |
|
収録物識別子 |
AA00664312 |
開始ページ |
|
|
開始ページ |
57 |
書誌情報 |
Hiroshima Journal of Medical Sciences
Hiroshima Journal of Medical Sciences
巻 49,
号 1,
p. 57-65,
発行日 2000-03
|
旧ID |
37702 |