ID | 61317 |
フルテキストURL | |
著者 |
Ikeda, A.
Department of Periodontics and Endodontics, Okayama University Hospital
Yamamoto, T.
Department of Pathophysiology - Periodontal Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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Mineshiba, J.
Hanamizuki Dental Clinic
Takashiba, S.
Department of Pathophysiology ‑ Periodontal Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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抄録 | Salivary glands (SGs) are very important for maintaining the physiological functions of the mouth. When SGs regenerate and repair from various damages, including mechanical, radiological, and immune diseases, acinar and granular duct cells originate from intercalated duct cells. However, the recovery is often insufficient because of SGs' limited self-repair function. Furthermore, the precise repair mechanism has been unclear. Here, we focused on CD49f, one of the putative stem cell markers, and characterized CD49f positive cells (CD49f(+) cells) isolated from male murine SGs. CD49f(+) cells possess self-renewal ability and express epithelial and pluripotent markers. Compared to CD49f negative cells, freshly isolated CD49f(+) cells highly expressed inhibin beta A and beta B, which are components of activin that has anti-proliferative effects. Notably, an inhibitor of activin, follistatin was expressed in mechanically-damaged SGs, meanwhile no follistatin was expressed in normal SGs in vivo. Moreover, sub-cultured CD49f(+) cells highly expressed both Follistatin and a series of proliferative genes, expressions of which were decreased by Follistatin siRNA. These findings indicated that the molecular interaction between activin and follistatin may induce CD49f(+) cells proliferation in the regeneration and repair of mouse SGs.
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発行日 | 2020-11-17
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出版物タイトル |
Scientific Reports
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巻 | 10巻
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号 | 1号
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出版者 | Nature Research
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開始ページ | 19959
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ISSN | 2045-2322
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資料タイプ |
学術雑誌論文
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言語 |
英語
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OAI-PMH Set |
岡山大学
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著作権者 | © The Author(s) 2020
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論文のバージョン | publisher
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PubMed ID | |
DOI | |
Web of Science KeyUT | |
関連URL | isVersionOf https://doi.org/10.1038/s41598-020-77004-2
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ライセンス | http://creat iveco mmons .org/licen ses/by/4.0/
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助成機関名 |
日本学術振興会
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助成番号 | 22792084
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