| 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 |
Role of the JNK pathway in thrombin-induced ICAM-1 expression in endothelial cells |
|
言語 |
en |
| 作成者 |
Miho, Narimasa
Ishida, Takafumi
Kuwada, Noriko
Ishida, Mari
Shimote, Keiko
Tabuchi, Kumiko
Oshima, Tetsuya
Yoshizumi, Masao
Chayama, Kazuaki
|
| 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 |
| 権利情報 |
|
|
権利情報 |
Copyright (c) 2005 European Society of Cardiology |
| 主題 |
|
|
主題Scheme |
Other |
|
主題 |
G proteins |
| 主題 |
|
|
主題Scheme |
Other |
|
主題 |
gene expression |
| 主題 |
|
|
主題Scheme |
Other |
|
主題 |
MAP kinase |
| 主題 |
|
|
主題Scheme |
Other |
|
主題 |
signal transduction |
| 主題 |
|
|
主題Scheme |
NDC |
|
主題 |
490 |
| 内容記述 |
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|
内容記述 |
Objective: Thrombin induces leukocyte adherence to endothelial cells via increased expression of intercellular adhesion molecule-1 (ICAM-1). Although ICAM-1 expression is regulated by NF-kappa B, recent studies have suggested that additional signaling mechanisms may also be involved. The goal of this study was to determine whether mitogen-activated protein (MAP) kinases, including extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), and p38 MAP kinase (p38), mediate thrombin-induced ICAM-1 expression in endothelial cells.Methods: Western blot analysis using anti-ICAM-1 antibody and luciferase assays were performed in cultured endothelial cells after addition of signal transduction inhibitors or transfection of various gene constructs. JNK kinase activity was determined by a kinase assay using c-Jun as a substrate or by Western blot analysis with anti-phospho-JNK antibody.Results: Treatment of endothelial cells with the JNK-specific inhibitors, SP600125 or JNK inhibitory peptide 1 (JNKI1), resulted in a significant decrease in thrombin-induced ICAM-1 expression as demonstrated by Western blot analysis (67 +/- 3 0x1.535a8bfffb01p-890nd 72 +/- 7%, respectively). In contrast, inhibitors of MEK and p38 had only minimal effect. The combination of SP600125 and the NF-kappa B inhibitor, BAY 11-7082, resulted in complete inhibition of thrombin-induced ICAM-1 expression. The G(alpha q) inhibitor, YM-254890, inhibited thrombin-induced JNK activation and ICAM-1 expression. Dominant-negative Ras and Rac1, but not Rho, inhibited thrombin-induced JNK activation and ICAM-1 promoter activity. Finally, thrombin-induced JNK activation and ICAM-1 promoter activity were inhibited by beta ARK1ct (a G beta gamma subunit scavenger) and Csk.Conclusions: These data suggest that, in concert with NF-kappa B, JNK regulates thrombin-induced ICAM-1 expression by a mechanism that is dependent on G(alpha q), G beta gamma, Ras, Rac1 and the Src kinase family. |
|
言語 |
en |
| 出版者 |
|
|
出版者 |
Oxford University 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 |
journal article |
| 出版タイプ |
|
|
出版タイプ |
AO |
|
出版タイプResource |
http://purl.org/coar/version/c_b1a7d7d4d402bcce |
| 関連情報 |
|
|
|
識別子タイプ |
DOI |
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|
関連識別子 |
10.1016/j.cardiores.2005.05.029 |
| 関連情報 |
|
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|
識別子タイプ |
PMID |
|
|
関連識別子 |
15979056 |
| 関連情報 |
|
|
関連タイプ |
isVersionOf |
|
|
識別子タイプ |
DOI |
|
|
関連識別子 |
http://dx.doi.org/10.1016/j.cardiores.2005.05.029 |
| 収録物識別子 |
|
|
収録物識別子タイプ |
NCID |
|
収録物識別子 |
AA0059904X |
| 収録物識別子 |
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|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
0008-6363 |
| 開始ページ |
|
|
開始ページ |
289 |
| 書誌情報 |
Cardiovascular Research
Cardiovascular Research
巻 68,
号 2,
p. 289-298,
発行日 2005-11-01
|
| 旧ID |
24937 |
CardioRes_68_289.pdf (1.6 MB)
