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〈原著〉脳由来神経栄養因子BDNFの心臓における発現と低酸素病態下での機能
https://kindai.repo.nii.ac.jp/records/20938
https://kindai.repo.nii.ac.jp/records/20938f127ae79-1f1e-4c8f-9353-c91720bb6b8a
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
AN00064044-20200331-0011.pdf (515.5 kB)
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| Item type | ☆紀要論文 / Departmental Bulletin Paper(1) | |||||||||||||||||
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| 公開日 | 2020-06-19 | |||||||||||||||||
| タイトル | ||||||||||||||||||
| タイトル | 〈原著〉脳由来神経栄養因子BDNFの心臓における発現と低酸素病態下での機能 | |||||||||||||||||
| タイトル | ||||||||||||||||||
| タイトル | 〈Original〉Functional role and expression of brain-derived neurotrophic factor (BDNF) in the heart exposed to hypoxia | |||||||||||||||||
| 言語 | en | |||||||||||||||||
| 著者 |
森島, 真幸
× 森島, 真幸
× 藤田, 崇史
× 小野, 克重
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| 言語 | ||||||||||||||||||
| 言語 | jpn | |||||||||||||||||
| キーワード | ||||||||||||||||||
| 主題 | Heart, BDNF, TrkB, hypoxia, T-type Ca2+ channel | |||||||||||||||||
| 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 | departmental bulletin paper | |||||||||||||||||
| 著者(英) | ||||||||||||||||||
| 言語 | en | |||||||||||||||||
| 値 | Morishima,Masaki | |||||||||||||||||
| 著者(英) | ||||||||||||||||||
| 言語 | en | |||||||||||||||||
| 値 | Fujita,Takafumi | |||||||||||||||||
| 著者(英) | ||||||||||||||||||
| 言語 | en | |||||||||||||||||
| 値 | Ono,Katsushige | |||||||||||||||||
| 著者 所属 | ||||||||||||||||||
| 値 | 近畿大学農学部食品栄養学科: 大分大学医学部病態生理学講座 | |||||||||||||||||
| 著者 所属 | ||||||||||||||||||
| 値 | 大分大学医学部病態生理学講座 | |||||||||||||||||
| 著者 所属 | ||||||||||||||||||
| 値 | 大分大学医学部病態生理学講座 | |||||||||||||||||
| 著者所属(翻訳) | ||||||||||||||||||
| 値 | Faculty of Agriculture, Kindai University: Department of Pathophysiology, Oita University School of Medicine | |||||||||||||||||
| 著者所属(翻訳) | ||||||||||||||||||
| 値 | Department of Pathophysiology, Oita University School of Medicine | |||||||||||||||||
| 著者所属(翻訳) | ||||||||||||||||||
| 値 | Department of Pathophysiology, Oita University School of Medicine | |||||||||||||||||
| 版 | ||||||||||||||||||
| 出版タイプ | NA | |||||||||||||||||
| 出版タイプResource | http://purl.org/coar/version/c_be7fb7dd8ff6fe43 | |||||||||||||||||
| 出版者 名前 | ||||||||||||||||||
| 出版者 | 近畿大学農学部 | |||||||||||||||||
| 書誌情報 |
近畿大学農学部紀要 en : MEMOIRS OF THE FACULTY OF AGRICULTURE OF KINDAI UNIVERSITY 号 53, p. 11-23, 発行日 2020-03-31 |
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| ISSN | ||||||||||||||||||
| 収録物識別子タイプ | ISSN | |||||||||||||||||
| 収録物識別子 | 21896267 | |||||||||||||||||
| 抄録 | ||||||||||||||||||
| 内容記述タイプ | Abstract | |||||||||||||||||
| 内容記述 | [Synopsis] Brain-derived neurotrophic factor (BDNF), conditionally secreted at active synapse through the stimulation of the tropomyosin-related kinase receptor B (TrkB) receptors, plays an important role in neuronal development, survival, and function. BDNF/TrkB signaling is reportedly essential for organ development or normal contractility in the mammalian heart. However, the expression patterns of BDNF/TrkB and their pathophysiologic roles are poorly understood in the heart. Here we report that BDNF/TrkB signaling is associated with cardiac automaticity in normal and hypoxic conditions. Expressions of BDNF and its receptor TrkB mRNAs in the atrium and the ventricle were abundant, which was approximately a half of those in brainstem or hippocampus, in an age-dependent manner. In hypoxic condition at 3 h (1%,O2), expression of BDNF mRNA was transiently activated in neonatal rat cardiomyocytes (126±7%), whereas this action was reduced (52±2%) at prolonged hypoxia (24 h). Reduction of the cellular automaticity, viability, and T-type Ca2+ channel expression by hypoxia were observed concomitantly with the inactivation of the BDNF/TrkB signal. Our data provide the first evidence that BDNF/TrkB signaling contributes to cardiac dysfunction under acute and prolonged hypoxia. | |||||||||||||||||
| フォーマット | ||||||||||||||||||
| 内容記述タイプ | Other | |||||||||||||||||
| 内容記述 | application/pdf | |||||||||||||||||
