Item type |
学術雑誌論文 / Journal Article(1) |
公開日 |
2023-05-30 |
タイトル |
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タイトル |
Omeprazole Suppresses Endothelial Calcium Response and eNOS Ser1177 Phosphorylation in Porcine Aortic Endothelial Cells |
言語 |
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言語 |
eng |
キーワード |
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主題 |
omeprazole |
キーワード |
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主題 |
nitric oxide synthase |
キーワード |
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主題 |
endothelial cells |
キーワード |
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主題 |
calcium |
キーワード |
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主題 |
endothelium-dependent relaxing factors |
資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
journal article |
著者 |
Kamiya, Chiaki
Odagiri, Keiichi
Hakamata, Akio
Sakurada, Ryugo
Inui, Naoki
Watanabe, Hiroshi
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書誌情報 |
Molecular Biology Reports
巻 48,
号 7,
p. 5503-5511,
発行日 2021-07
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出版者 |
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出版者 |
Springer Nature |
権利 |
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権利情報 |
This version of the article has been accepted for publication, after peer review (when applicable) and is subject to Springer Nature’s AM terms of use, but is not the Version of Record and does not reflect post-acceptance improvements, or any corrections. The Version of Record is available online at: http://dx.doi.org/10.1007/s11033-021-06561-0 |
抄録 |
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内容記述タイプ |
Abstract |
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内容記述 |
Background Although high doses of proton pump inhibitors can elicit an anticancer effect, this strategy may impair vascular biology. In particular, their effects on endothelial Ca2⁺ signaling and production of endothelium-derived relaxing factor (EDRF) are unknown. To this end, we investigated the effects of high dosages of omeprazole on endothelial Ca2⁺ responses and EDRF production in primary cultured porcine aortic endothelial cells. Methods and Results Omeprazole (10–1000μM) suppressed both bradykinin (BK)- and thapsigargin-induced endothelial Ca2⁺ response in a dose-dependent manner. Furthermore, omeprazole slightly attenuated Ca2⁺ mobilization from the endoplasmic reticulum, whereas no inhibitory effects on endoplasmic reticulum Ca2⁺-ATPase were observed. Omeprazole decreased BK-induced phosphorylation of endothelial nitric oxide synthase (eNOS) at Ser1177 and tended to decrease BK-induced nitric oxide production. Production of prostaglandin I₂ metabolites, especially 6-keto-prostaglandin 1α, also tended to be reduced by omeprazole. Conclusion Our results are the first to indicate that high doses of omeprazole may suppress both store-operated Ca2⁺ channels and partially the G protein-coupled receptor/phospholipase C/inositol 1,4,5-triphosphate pathway, and decreased BKinduced, Ca2⁺-dependent phosphorylation of eNOS(Ser1177). Thus, high dosages of omeprazole impaired EDRF production by attenuating intracellular Ca2⁺ signaling. |
ISSN |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
0301-4851 |
EISSN |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
1573-4978 |
NII書誌ID |
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収録物識別子タイプ |
NCID |
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収録物識別子 |
AA00745797 |
PubMed番号 |
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関連タイプ |
isVersionOf |
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識別子タイプ |
PMID |
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関連識別子 |
34291395 |
出版社DOI |
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関連タイプ |
isVersionOf |
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識別子タイプ |
DOI |
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関連識別子 |
10.1007/s11033-021-06561-0 |
著者版フラグ |
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出版タイプ |
AM |
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出版タイプResource |
http://purl.org/coar/version/c_ab4af688f83e57aa |