Functional roles of RhoT1 on repair of periodontal tissue
| Project/Area Number |
15K11028
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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 |
Morphological basic dentistry
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| Research Institution | Nihon University (2017)
Matsumoto Dental University (2015-2016) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
小出 雅則 松本歯科大学, 総合歯科医学研究所, 講師 (10367617)
中村 浩彰 松本歯科大学, 歯学部, 教授 (50227930)
平賀 徹 松本歯科大学, 歯学部, 准教授 (70322170)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | RhoT1 / MSCs / 遊走能 / ミトコンドリア / ミトコンドリア輸送 / MSC / 間葉系幹細胞 / 細胞遊走 / 歯学 / 細胞・組織 |
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| Outline of Final Research Achievements |
This study aimed to elucidate the functional role of mitochondrial Rho GTPase 1 (RhoT1), mitochondrial transporter factor, on the repair of periodontal tissue. RhoT1 expressed on mesenchymal stromal cells (MSCs) in periodontal ligament (PDL) and the level of its expression increased with stimulation of LPS and starvation state. In addition, damaged PDL MSCs were rescued by a transport of mitochondria from intact PDL MSCs and then were survived. These finding indicated that RhoT1 is important for restoring the damage of periodontal ligament cells.
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Report
(4 results)
Research Products
(34 results)
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[Journal Article] A Jak1/2 inhibitor, baricitinib, inhibits osteoclastogenesis by suppressing RANKL expression in osteoblasts in vitro.2017
Author(s)
Murakami K, Kobayashi Y, Uehara S, Suzuki T, Koide M, Yamashita T, Nakamura M, Takahashi N, Kato H, Udagawa N and Nakamura Y
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Journal Title
PLOS ONE
Volume: 12
Issue: 7
Pages: e0181126-e0181126
DOI
Related Report
Peer Reviewed / Open Access
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