| Project/Area Number |
25463037
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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 | Tsurumi University |
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Principal Investigator |
SUGA Takeo 鶴見大学, 歯学部, 講師 (40247333)
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| Co-Investigator(Kenkyū-buntansha) |
OGAWA Takumi 鶴見大学, 歯学部, 教授 (20267537)
ANDO Hitoshi 鶴見大学, 歯学部, 講師 (00282765)
山根 明 鶴見大学, 歯学部, 教授 (20166763)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | miR-206 / miR-29 / mi/mi mouse / 咬筋 / アセチルコリン受容体 / miR-29a / 非咬合マウス / mi/miマウス / ACh受容体 / Ach受容体 |
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| Outline of Final Research Achievements |
Expression of endogenous miR-206 markedly increased with a peak at 4 weeks in the masseter of wild mice, but it kept low level until 12 weeks in those of the mi/mi mice. It suggested that miR-206 has a role in the formation of ACh receptor clusters. However, The average number of ACh receptor clusters was not changed when expression of miR-206 was inhibited or enhanced. More successful method of loss and gain of function experiments for microRNAs. We also investigated expression change of miR-29a which is another important microRNA in mygenesis. Expression pattern of miR-29a was similar to miR-206, but it could not change expressions of Agrin, MuSK, Lrp4 and Rapsin, which are regulation genes of ACh reseptor cluster formation.
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