Functional elucidation of Runx2 for pathological analysis in delay of orthodontic tooth movement in Cleidocranial dysplasia
| Project/Area Number |
26861768
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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 | Tohoku University |
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Principal Investigator |
AONUMA TOMO 東北大学, 歯学研究科(研究院), 大学院非常勤講師 (70624823)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | Runx2 / メカニカルストレス / 細胞増殖 / メカノトランスダクション |
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| Outline of Final Research Achievements |
Runx2, is an essential transcription factor of osteoblast differentiation, is important for mechanotransduction. Tooth movement in cleidocranial dysplasia(CCD), caused by Runx2 gene mutation,is delayed. Our group found delayed tooth movement and reduction of response for mechanical stress in periodontal tissue of Runx2+/- mice, animal model of CCD. Because of reduction of bone formation in tension side of tooth movement, we investigated proliferation of bone marrow stromal cells after stretch. We found cell proliferation in Runx2+/- mice by stretch was decreased compared with wild-type mice(WT). We found strong phosphorylation of ERK in stretched cells from WT, but no change in Runx2+/- mice. Stretch did not change phospho-p38 and JNK in both mice. Although strong phosphorylation of ERK by stretch was required in stretched cells from WT, but not Runx2+/- mice. Thus, possibility of reduction of function of mechanical stress pathways in Runx2+/- mice has been suggested.
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Report
(3 results)
Research Products
(3 results)
