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Intracellular renin protects cardiomyocytes from ischemic injury in diabetic heart
http://hdl.handle.net/10271/3138
http://hdl.handle.net/10271/31381098cb47-941b-47bd-a049-cb059fc2721c
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
論文本文 (1.1 MB)
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| Item type | 学位論文 / Thesis or Dissertation(1) | |||||
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| 公開日 | 2017-01-28 | |||||
| タイトル | ||||||
| タイトル | Intracellular renin protects cardiomyocytes from ischemic injury in diabetic heart | |||||
| 言語 | en | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | Renin | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | Diabetes mellitus | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | Ischemia | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | Mitochondria | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | Direct renin inhibitor | |||||
| 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 | 細胞内レニンは糖尿病心の虚血傷害から心筋細胞を保護する | |||||
| 言語 | ja | |||||
| 著者 |
Nonaka, Daishi
× Nonaka, Daishi |
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| 書誌情報 |
en : Journal of Cardiovascular Diseases & Diagnosis 巻 3, 号 4, p. 1000214, 発行日 2015-07-31 |
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| 出版者 | ||||||
| 出版者 | OMICS International | |||||
| 言語 | en | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Background: Local Renin-Angiotensin-Aldosterone system (RAS) is important in cardiac pathophysiology. We investigated the expression and distribution of intracellular renin after ischemia, and the effects of renin on mitochondrial function in diabetic heart. Methods: In Goto-Kakizaki (DM) and Wistar (non-DM) rats, Langendorff-perfused hearts were subjected to ischemia by coronary artery ligation for 90 min. Infarct Size (IS) and expression of RAS components were examined. Mitochondrial membrane potential (ΔΨm), uncoupling protein-2 (UCP2), NAD/NADH ratio, and ATP were measured in renin-treated myocytes or isolated mitochondria. Results: After ischemia, LV function (LVDP; 76 ± 4 vs. 52 ± 4 mmHg, LVEDP; 18 ± 2 vs. 29 ± 4 mmHg, p<0.05, DM; n=9, non-DM; n=9, respectively) was prevented and IS (44.2 ± 2.1 vs. 53.7 ± 2.9 %, p<0.05) was significantly small in DM hearts. These cardioprotective effects were abolished when DM hearts were treated with direct renin inhibitor (LVDP; 77 ± 3 vs. 55 ± 4 mmHg, LVEDP; 16 ± 1 vs. 27 ± 3 mmHg, IS; 40.8 ± 2.9 vs. 52.1 ± 3.4 %, p<0.05, DM; n=5, DM plus DRI; n=5, respectively). Renin expression in the ischemic area was increased in DM hearts. Electron microscopy showed predominant renin localization within mitochondria. In permeabilized myocytes or isolated mitochondria, renin hyperpolarized ΔΨm, increased NAD/NADH ratio and preserved ATP content. Ischemiainduced UCP2 expression was reduced in DM. Conclusions: Intracellular renin, which mainly localizes within mitochondria, increased during ischemia and protected cardiomyocytes in diabetic hearts. This protective effect of renin is at least partially because of the reduction of UCP2 and the acceleration of electron transport chain, which resulted in the prevention of mitochondrial depolarization and ATP production. |
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| 言語 | en | |||||
| 学位名 | ||||||
| 言語 | ja | |||||
| 学位名 | 博士（医学） | |||||
| 学位の区分 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | doctoral | |||||
| 言語 | en | |||||
| 学位の分野 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 医学系研究科 | |||||
| 言語 | ja | |||||
| 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 | |||||
| 言語 | ja | |||||
| 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 | 2016-03-14 | |||||
| 学位授与番号 | ||||||
| 学位授与番号 | 甲第716号 | |||||
| ISSN | ||||||
| 収録物識別子タイプ | PISSN | |||||
| 収録物識別子 | 2329-9517 | |||||
| 出版社DOI | ||||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | https://doi.org/10.4172/2329-9517.1000214 | |||||
| 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 | |||||
