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Linoleic acid attenuates endothelium-derived relaxing factor production by suppressing cAMP-hydrolyzing phosphodiesterase activity
http://hdl.handle.net/10271/2877
http://hdl.handle.net/10271/2877f488fcee-59d9-4f3e-99e0-a3775400f5c9
| 名前 / ファイル | ライセンス | アクション |
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論文本文 (1.5 MB)
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| Item type | 学位論文 / Thesis or Dissertation(1) | |||||||
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| 公開日 | 2015-08-11 | |||||||
| タイトル | ||||||||
| タイトル | Linoleic acid attenuates endothelium-derived relaxing factor production by suppressing cAMP-hydrolyzing phosphodiesterase activity | |||||||
| 言語 | en | |||||||
| 言語 | ||||||||
| 言語 | eng | |||||||
| キーワード | ||||||||
| 主題 | Cyclic AMP | |||||||
| キーワード | ||||||||
| 主題 | Endothelial cells | |||||||
| キーワード | ||||||||
| 主題 | Endothelium-derived relaxing factor | |||||||
| キーワード | ||||||||
| 主題 | Linoleic acid | |||||||
| キーワード | ||||||||
| 主題 | Phosphdiesterase | |||||||
| 資源タイプ | ||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_db06 | |||||||
| 資源タイプ | doctoral thesis | |||||||
| 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 | |||||||
| その他のタイトル | ||||||||
| その他のタイトル | リノール酸はcAMP加水分解型ホスホジエステラーゼ阻害を介して内皮由来血管弛緩因子産生を抑制する | |||||||
| 著者 |
韦, 嘉章
× 韦, 嘉章
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| 書誌情報 |
en : Circulation Journal 巻 77, 号 11, p. 2823-2830, 発行日 2013-11 |
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| 出版者 | ||||||||
| 出版者 | 日本循環器学会 | |||||||
| 出版者 | ||||||||
| 出版者 | The Japanese Circulation Society | |||||||
| 抄録 | ||||||||
| 内容記述タイプ | Abstract | |||||||
| 内容記述 | Background: Linoleic acid (LA) promotes monocyte chemotaxis and cell adhesion molecules such as MCP-1 and VCAM-1, which contribute to atherosclerogenesis. These molecules are restrained by endothelium-derived relaxing factors (EDRFs), such as nitric oxide (NO) and prostaglandin I2 (PGI2). Hence, the expressions of MCP-1 and VCAM-1 upregulated by LA may be partly attributable to decreased EDRF production. However, effect of LA on EDRF production remains controversial. Methods and Results: The present study aimed to examine the effects of LA and other free fatty acids on EDRF production and the endothelial Ca2+ responses that mediate EDRF production, using primary cultured porcine aortic endothelial cells (PAECs). LA at 0.1-5μmol/L attenuated bradykinin (BK)-induced NO and PGI2 production while suppressing the BK-induced Ca2+ response dose-dependently. The inhibitory effect of LA on the Ca2+ response was eliminated by adenylate cyclase inhibitor SQ22536, boosted by cAMP-hydrolyzing phosphodiesterase (PDE) inhibitor, rolipram, and mimicked by plasma membrane permeable 8-bromo-cAMP. Moreover, LA was confirmed to dose-dependently increase intracellular cAMP levels and selectively inhibit cAMP-hydrolyzing PDE activity in vitro. In contrast, none of palmitic, stearic, or oleic acid affected BK-induced EDRF production or Ca2+ responses, or induced intracellular cAMP accumulation. Conclusions: LA induced intracellular cAMP accumulation by inhibiting cAMP-hydrolyzing PDE activity, thus resulting in attenuation of Ca2+ responses and EDRF production in PAECs. |
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| 言語 | en | |||||||
| 学位名 | ||||||||
| 学位名 | 博士（医学） | |||||||
| 学位の区分 | ||||||||
| 内容記述 | doctoral | |||||||
| 学位の分野 | ||||||||
| 内容記述 | 医学系研究科 | |||||||
| 学位授与機関 | ||||||||
| 学位授与機関識別子Scheme | kakenhi | |||||||
| 学位授与機関識別子 | 13802 | |||||||
| 学位授与機関名 | 浜松医科大学 | |||||||
| 学位授与年月日 | ||||||||
| 学位授与年月日 | 2014-09-19 | |||||||
| 学位授与番号 | ||||||||
| 学位授与番号 | 甲第685号 | |||||||
| ISSN | ||||||||
| 収録物識別子タイプ | PISSN | |||||||
| 収録物識別子 | 1346-9843 | |||||||
| EISSN | ||||||||
| 収録物識別子タイプ | EISSN | |||||||
| 収録物識別子 | 1347-4820 | |||||||
| PubMed番号 | ||||||||
| 識別子タイプ | PMID | |||||||
| 関連識別子 | 23883876 | |||||||
| 出版社DOI | ||||||||
| 識別子タイプ | DOI | |||||||
| 関連識別子 | https://doi.org/10.1253/circj.CJ-13-0248 | |||||||
| 著者版フラグ | ||||||||
| 出版タイプ | VoR | |||||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||||
