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ファイル | 記述 | サイズ | フォーマット | |
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j.stemcr.2016.05.015.pdf | 3.17 MB | Adobe PDF | 見る/開く |
タイトル: | Dopamine D2 Receptor-Mediated Regulation of Pancreatic β Cell Mass |
著者: | Sakano, Daisuke Choi, Sungik Kataoka, Masateru Shiraki, Nobuaki Uesugi, Motonari https://orcid.org/0000-0002-8515-445X (unconfirmed) Kume, Kazuhiko Kume, Shoen |
著者名の別形: | 上杉, 志成 |
発行日: | 12-Jul-2016 |
出版者: | Elsevier BV |
誌名: | Stem cell reports |
巻: | 7 |
号: | 1 |
開始ページ: | 95 |
終了ページ: | 109 |
抄録: | Understanding the molecular mechanisms that regulate β cell mass and proliferation is important for the treatment of diabetes. Here, we identified domperidone (DPD), a dopamine D2 receptor (DRD2) antagonist that enhances β cell mass. Over time, islet β cell loss occurs in dissociation cultures, and this was inhibited by DPD. DPD increased proliferation and decreased apoptosis of β cells through increasing intracellular cAMP. DPD prevented β cell dedifferentiation, which together highly contributed to the increased β cell mass. DRD2 knockdown phenocopied the effects of domperidone and increased the number of β cells. Drd2 overexpression sensitized the dopamine responsiveness of β cells and increased apoptosis. Further analysis revealed that the adenosine agonist 5′-N-ethylcarboxamidoadenosine, a previously identified promoter of β cell proliferation, acted with DPD to increase the number of β cells. In humans, dopamine also modulates β cell mass through DRD2 and exerts an inhibitory effect on adenosine signaling. |
著作権等: | © 2016 The Author(s). This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
URI: | http://hdl.handle.net/2433/216336 |
DOI(出版社版): | 10.1016/j.stemcr.2016.05.015 |
PubMed ID: | 27373926 |
出現コレクション: | 学術雑誌掲載論文等 |
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