| Project/Area Number |
16K11580
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Prosthodontics/ Dental materials science and
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| Research Institution | Tohoku Fukushi University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
神崎 展 東北大学, 医工学研究科, 准教授 (10272262)
渡邉 誠 東北福祉大学, その他, 教授 (80091768)
萩原 嘉廣 東北大学, 医学系研究科, 准教授 (90436139)
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| Project Period (FY) |
2016-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 顎関節症 / 好中球 / IL1 / 糖代謝 / 筋衛星細胞 / IL-1 / 慢性筋痛 / 筋細胞融合 / 筋痛 |
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| Outline of Final Research Achievements |
Skeletal muscle regeneration after injury is a complex process involving inflammatory microenvironments. Interleukin (IL)-1 is a key mediator of inflammatory responses and exerts pleiotropic impacts on various cell types. Thus, we aimed to investigate the role of IL-1 during skeletal muscle regeneration. We herein show that IL-1KO mice exhibit delayed muscle regeneration characterized by delayed infiltrations of immune cells accompanied by suppressed local production of proinflammatory factors including IL-6 and delayed increase of satellite cells postinjury. Meanwhile, IL-1β secretion and NLRP3 inflammasome activation in macrophages produced mechanical hyperalgesia on over-exercised muscle pain. Taken together, we conclude that IL-1 plays a positive role in muscle regeneration, but also reduces over-exercised muscle pain.
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| Academic Significance and Societal Importance of the Research Achievements |
顎関節症に伴う慢性筋痛の多くは筋・筋膜性疼痛疾患(MPS)と同様の症状を含み，異常な線維性構造（索状硬結）の存在と遷延化した炎症性サイトカイン産生を特徴とする．しかしながら，その発症メカニズムは不明であり，治療法も確立されていない．
運動後の筋組織ではIL1βの発現上昇と細胞融合の活性化が報告されている．本研究ではその現象に着目し，運動後に浸潤する炎症性細胞がIL-1βを介して筋痛を誘導することを明らかとした．IL-1は主要な炎症性サイトカインとしての働きが知られる一方で、そのメカニズムについては不明な点が多いが、我々の結果はIL-1の新規性のある働きを示すものである．
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