| Project/Area Number |
25670885
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Periodontology
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| Research Institution | Hiroshima University |
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Principal Investigator |
KURIHARA HIDEMI 広島大学, 医歯薬保健学研究院, 教授 (40161765)
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| Co-Investigator(Kenkyū-buntansha) |
UCHIDA Yuushi 広島大学, 医歯薬保健学研究院(歯), 助教 (40363080)
FUJITA Tsuyoshi 広島大学, 病院, 講師 (80379883)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | ペリオスチン / 歯肉上皮 / E-cadherin / アポトーシス / smad2 / TGF-beta / 歯肉上皮細胞 / apoptosis / 歯周炎 / マウス |
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| Outline of Final Research Achievements |
Periostin suppresed the expression of E-cadherin in human gingival epithelial cells, suggesting that periostin down-regulate the barrier function of gingival epithelium. Since it has been reported that periostin secreted from epithelial cells activates TGF signaling, we examined the effect of TGF-beta on apoptosis of epithelial cells. The results showed TGF-beta induced mitochondria-dependent apoptosis in huma gingival epithelail cells. As apoptosis is known to induce the reduction of epithelail barrier, it may be suggested that TGF-beta/smad2 signaling and apoptosis are involved in the periostin-indueeced suppression of epithelial barrier.
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