Inhibition of ADAM10 in satellite cells accelerates muscle regeneration following muscle injury
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- Sakiko Mizuno
- Department of Orthopedic Surgery Keio University School of Medicine 35 Shinanomachi Shinjuku‐ku Tokyo 160‐8582 Japan
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- Masaki Yoda
- Laboratory of Cell and Tissue Biology Keio University School of Medicine 35 Shinanomachi Shinjuku‐ku Tokyo 160‐8582 Japan
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- Masayuki Shimoda
- Department of Pathology Keio University School of Medicine 35 Shinanomachi Shinjuku‐ku Tokyo 160‐8582 Japan
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- Kazuhiro Chiba
- Department of Orthopedic Surgery National Defense Medical College Namiki 3‐2 Tokorozawa Saitama 359‐8513 Japan
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- Masaya Nakamura
- Department of Orthopedic Surgery Keio University School of Medicine 35 Shinanomachi Shinjuku‐ku Tokyo 160‐8582 Japan
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- Keisuke Horiuchi
- Department of Orthopedic Surgery Keio University School of Medicine 35 Shinanomachi Shinjuku‐ku Tokyo 160‐8582 Japan
書誌事項
- 公開日
- 2018-03-14
- 資源種別
- journal article
- 権利情報
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- http://onlinelibrary.wiley.com/termsAndConditions#vor
- DOI
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- 10.1002/jor.23878
- 公開者
- Wiley
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説明
<jats:title>ABSTRACT</jats:title><jats:sec><jats:label/><jats:p>Muscle injury is one of the most common orthopedic and sports disorders. For severe cases, surgical repair may be indicated; however, other than immobilization and the administration of anti‐inflammatory drugs there is currently no effective conservative treatment for this condition. Satellite cells (SCs) are muscle‐specific stem cells and are indispensable for muscle regeneration after muscle injury. SCs are activated upon muscle injury to proliferate and differentiate into myoblasts, which subsequently fuse into myofibers and regenerate the damaged muscle. We have previously shown that ADAM10, a membrane‐anchored proteolytic enzyme, is essential for the maintenance of SC quiescence by activating the Notch signaling pathway in SCs. Because suppression of ADAM10 activity in SCs can activate SC differentiation, we asked whether inactivation of ADAM10 in SCs after muscle injury could enhance muscle regeneration. Using <jats:italic>Adam10</jats:italic> conditional knockout mice, in which ADAM10 activity can specifically be suppressed in SCs, we found that partial inactivation of ADAM10 accelerates muscle regeneration after muscle injury. Nearly identical results were obtained by the administration of GI254023X, a selective ADAM10 inhibitor. The findings of the present study thus indicate that transient enhancement of SC differentiation after muscle injury expedites muscle regeneration and that ADAM10 can be a potential molecular target in treating muscle injuries. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:2259–2265, 2018.</jats:p></jats:sec>
収録刊行物
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- Journal of Orthopaedic Research
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Journal of Orthopaedic Research 36 (8), 2259-2265, 2018-03-14
Wiley