| Project/Area Number |
26861803
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Orthodontics/Pediatric dentistry
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| Research Institution | Tsurumi University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2016: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2015: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2014: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
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| Keywords | 咀嚼筋 / シグナル伝達 / デキサメタゾン / 筋萎縮 / 筋線維タイプ / 筋肥大 / マイクロRNA |
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| Outline of Final Research Achievements |
Masticatory muscles have the potential to adapt their mass and fiber types to a wide range of functional demands, as observed in limb muscles. However, these molecular mechanisms are poorly understood. In this study, we analyzed the effects of bite-opening treatment (BO) on muscle phenotypes of mice masseter muscle. To examine hypertrophic effects of BO on masseter and soleus muscles as well as antagonistic action of dexamethasone (DEX), a glucocorticoid, against hypertrophy, we analyzed both muscle mass and fiber diameter of masseter, soleus muscles in BO and/or DEX-treated mice. These results suggest that differences in the sensitivity to DEX or in the mechanisms of DEX antagonism between masseter and soleus muscles.
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