| Project/Area Number |
25293371
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Niigata University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TSUJIGIWA Hidetsugu 岡山理科大学, 理学部, 教授 (70335628)
HONDA Masaki 愛知学院大学, 歯学部, 教授 (70361623)
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| Co-Investigator(Renkei-kenkyūsha) |
IDA Hiroko (YONEMOCHI Hiroko) 新潟大学, 医歯学系, 准教授 (60293213)
NAKATOMI Mitsushiro 九州歯科大学, 歯学部, 講師 (10571771)
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| Research Collaborator |
SAITO Kotaro 新潟大学, 医歯学系, 助教 (10733719)
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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 |
¥17,550,000 (Direct Cost: ¥13,500,000、Indirect Cost: ¥4,050,000)
Fiscal Year 2015: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2014: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥8,710,000 (Direct Cost: ¥6,700,000、Indirect Cost: ¥2,010,000)
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| Keywords | 歯髄 / 静的幹細胞 / 前駆細胞 / 再植・移植 / 幹細胞ニッチ / 長期ラベル細胞 / 象牙芽細胞様細胞 / TetOP-H2B-GFPマウス / 歯髄幹細胞 / H2B-GFPマウス / BrdUラベル保持細胞 / ソニックヘッジホッグ / GFP骨髄移植マウス |
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| Outline of Final Research Achievements |
Long term label-retaining cells (LRCs) were localized in the subodontoblastic layer as well as the perivascular niche in the center of dental pulp, demonstrated by TetOP-H2B-GFP mutant mice that allow doxycycline-inducible, green fluorescent labeling of cells. The disappearance of LRCs was attributed to the extensive apoptosis occurring significantly in LRCs except for the newly-differentiated odontoblast-like cells even in cases without immunological rejection in the process of pulpal healing following allogenic tooth transplantation. Microarray and immunohistochemical analyses demonstrated that insulin-like growth factor binding protein (IGFBP) 5 is supposed to pay an important role in the maintenance of quiescent dental pulp stem/progenitor cells. Furthermore, the co-localization of transcriptional factor Gli1 and receptor Patched1 in the quiescent stem cells suggests that these cells are regulated by sonic hedgehog signaling.
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