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  1. 学術雑誌論文
  2. 各雑誌掲載論文

Omeprazole Suppresses Endothelial Calcium Response and eNOS Ser1177 Phosphorylation in Porcine Aortic Endothelial Cells

http://hdl.handle.net/10271/00004367
http://hdl.handle.net/10271/00004367
ba2bf9d4-22ea-4b5b-a25b-523f8840cc80
名前 / ファイル ライセンス アクション
Mol.Bio.Rep.-48-5503.pdf Mol.Bio.Rep.-48-5503.pdf (1.9 MB)
Item type 学術雑誌論文 / Journal Article(1)
公開日 2023-05-30
タイトル
タイトル Omeprazole Suppresses Endothelial Calcium Response and eNOS Ser1177 Phosphorylation in Porcine Aortic Endothelial Cells
言語
言語 eng
キーワード
主題 omeprazole
キーワード
主題 nitric oxide synthase
キーワード
主題 endothelial cells
キーワード
主題 calcium
キーワード
主題 endothelium-dependent relaxing factors
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
著者 Kamiya, Chiaki

× Kamiya, Chiaki

Kamiya, Chiaki

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Odagiri, Keiichi

× Odagiri, Keiichi

Odagiri, Keiichi

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Hakamata, Akio

× Hakamata, Akio

Hakamata, Akio

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Sakurada, Ryugo

× Sakurada, Ryugo

Sakurada, Ryugo

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Inui, Naoki

× Inui, Naoki

Inui, Naoki

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Watanabe, Hiroshi

× Watanabe, Hiroshi

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
出版者
出版者 Springer Nature
権利
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
内容記述タイプ Abstract
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
収録物識別子タイプ ISSN
収録物識別子 0301-4851
EISSN
収録物識別子タイプ ISSN
収録物識別子 1573-4978
NII書誌ID
収録物識別子タイプ NCID
収録物識別子 AA00745797
PubMed番号
関連タイプ isVersionOf
識別子タイプ PMID
関連識別子 34291395
出版社DOI
関連タイプ isVersionOf
識別子タイプ DOI
関連識別子 10.1007/s11033-021-06561-0
著者版フラグ
出版タイプ AM
出版タイプResource http://purl.org/coar/version/c_ab4af688f83e57aa
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