Intracellular renin protects cardiomyocytes from ischemic injury in diabetic heart 4

• Material Type: 博士論文
• Title: Intracellular renin protects cardiomyocytes from ischemic injury in diabetic heart
• Volume: 3 4
• Author/Editor: Nonaka, Daishi
• Author Heading: Nonaka, Daishi
• Publication, Distribution, etc.: OMICS International
• Publication Date: 2015-07-31
• Publication Date (W3CDTF): 2015-07-31
• Alternative Title: 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
• Periodical title: Journal of Cardiovascular Diseases & Diagnosis
• Degree grantor/type: 浜松医科大学
• Date Granted: 2016-03-14
• Date Granted (W3CDTF): 2016-03-14
• Dissertation Number: 甲第716号
• Degree Type: 博士（医学）
• Conferring No. (Dissertation): 甲第716号
• Text Language Code: eng
• Subject Heading: Renin; Diabetes mellitus; Ischemia; Mitochondria; Direct renin inhibitor
• Target Audience: 一般
• Note (General): doctoral; 医学系研究科; 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.
• DOI: info:doi/10.4172/2329-9517.1000214; https://doi.org/info:doi/10.4172/2329-9517.1000214
• Persistent ID (NDL): info:ndljp/pid/10300476; https://dl.ndl.go.jp/pid/10300476
• Collection: 障害者向け資料
• Collection (Materials For Handicapped People:1): テキストデータ
• Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• Acquisition Basis: 博士論文（自動収集）
• Date Accepted (W3CDTF): 2017-02-09T20:08:30+09:00
• Date Created (W3CDTF): 2018-08-27
• Format (IMT): application/pdf
• Access Restrictions: 国立国会図書館内限定公開
• Service for the Digitized Contents Transmission Service: 図書館・個人送信対象外
• Availability of remote photoduplication service: 可
• Periodical Title (URI): http://hdl.handle.net/10271/3138; https://hama-med.repo.nii.ac.jp/records/2996
• Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp

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