2012 Fiscal Year Final Research Report
Regulatory mechanisms of bone metabolism by nervous system
| Project/Area Number |
20591790
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Saitama Medical University |
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Principal Investigator |
KATO Naoki 埼玉医科大学, 医学部, 講師 (90448895)
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| Co-Investigator(Renkei-kenkyūsha) |
MATSUMOTO Masahito 埼玉医科大学, 医学部, 講師 (90321819)
ODA Hiromi 埼玉医科大学, 医学部, 教授 (60101698)
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| Project Period (FY) |
2008 – 2012
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| Keywords | シグナル伝達 / 酵素 / 転写因子 / 骨代謝 / 神経科学 |
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| Research Abstract |
We generated novel p38αmutant mice (sem mice) with a point mutation in the region encoding the p38αsubstrate-docking-site, which serves as a limited loss-of-function model of p38α. In the present study, we utilized sem mice and wild-type littermates (wt mice) to investigate the physiological role of p38αin bone metabolism and in nerve regeneration. In bone metabolism, sem mice showed higher bone density compared with wt mice, which could come from the inhibition of the osteoclast differentiation. In nerve regeneration, we confirmed that histological and functional nerve recovery following crush injury was delayed in sem mice compared with that in wt mice. To investigate the underlying mechanisms of these findings, we examined inflammatory responses of the sciatic nerve, and found that TNF-α, IL-1β, Caspase-3 and Tenascin-C showed different expression patterns following crush injury. This is the first study demonstrating physiological role of p38αin bone metabolism and in nerve regeneration without the use of pharmacological inhibitors.
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