| Project/Area Number |
24890008
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Surgical dentistry
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| Research Institution | Hokkaido University |
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Principal Investigator |
ASAKA Takuya 北海道大学, 歯学研究科(研究院), 助教 (80637265)
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| Project Period (FY) |
2012-08-31 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | ７型コラーゲン / エナメル芽細胞 / トームス突起 / エナメル小柱 |
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| Research Abstract |
Recessive dystrophic epidermolysis bullosa (RDEB) is caused by mutations in the gene encoding type VII collagen (COL7), a major component of anchoring fibrils in the epidermal basement membrane zone. We examined the tooth enamel structure of an RDEB patient by scanning electron microscopy. It showed irregular enamel prisms, indicating structural enamel defects. The enamel calcification and chemical composition of Col7a1-/- mice were similar to those of the wild type. However, transverse sections of teeth from the Col7a1-/- mice showed irregular enamel prisms, which were also observed in the RDEB patient.Furthermore, the Col7a1-/- mice teeth had poorly differentiated ameloblasts, lacking normal enamel protein-secreting Tomes processes, and showed reduced mRNA expression of amelogenin and other enamel-related molecules. These findings suggest that COL7 regulates ameloblast differentiation and is essential for the formation of Tomes processes.
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