Project/Area Number |
16K11804
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Orthodontics/Pediatric dentistry
|
Research Institution | The University of Tokushima |
Principal Investigator |
HASEGAWA Tomokazu 徳島大学, 大学院医歯薬学研究部(歯学域), 講師 (50274668)
|
Co-Investigator(Kenkyū-buntansha) |
吉村 善隆 北海道大学, 歯学研究院, 准教授 (30230816)
|
Project Period (FY) |
2016-10-21 – 2020-03-31
|
Project Status |
Completed (Fiscal Year 2019)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
Keywords | 歯周組織 / 歯髄組織 / 歯根膜細胞 / 歯髄細胞 / エピジェネティクス / 低酸素培養 / 矯正治療 / 脱メチル化 / 歯根膜 / 乳歯 / 恒常性 / 顎口腔系歯学 |
Outline of Final Research Achievements |
To elucidate the maintenance of homeostasis and mechanism of regenerative medicine in periodontal tissues, we studied the effect of FGF-2 on expression of SDF-1α and CCL11 using with periodontal ligament (PDL) cells and pulp cells derived from deciduous teeth. Although it has been showed that FGF-2 could affect many effective function on PDL tissues and pulp tissues, both cells had expressed decreasing expression of SDF-1α which could induce migration of mesenchymal stem cells concentration-dependency manner treating with FGF-2. Together with the results of epigenetics of PDL cells in hypoxia, there are many systems for the maintenance of homeostasis and mechanism of regenerative medicine in PDL tissue and pulp tissue. Therefore,, we should choose adequate strategies for therapies of dental disease.
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Academic Significance and Societal Importance of the Research Achievements |
歯周組織や歯の恒常性維持機構・再生機構の解析において、歯根膜細胞および歯髄細胞において組織再生に有利なケモカインや、炎症反応に関与すると考えられるケモカインの発現調節機構について解析を行った。本申請の研究結果から歯根膜や歯髄組織において、サイトカインによる受容体から細胞内シグナルを介した直接的な遺伝子の発現調節機構だけでなく、他のサイトカインの受容体発現を抑制して二次的に遺伝子の発現を調節する機構も示唆された。さらにDNAの脱メチル化機構により遺伝子の発現調節が行われている可能性も示唆された。
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