| Project/Area Number |
16K11789
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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 |
Orthodontics/Pediatric dentistry
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| Research Institution | Hiroshima University |
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Principal Investigator |
HIROSE NAOTO 広島大学, 医系科学研究科(歯), 助教 (50611935)
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| Co-Investigator(Kenkyū-buntansha) |
國松 亮 広島大学, 病院(歯), 講師 (40580915)
吉見 友希 広島大学, 病院(歯), 病院助教 (50707081)
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| Research Collaborator |
SUMI Chikako
YANOSHITA Makoto
TAKANO Mami
NISHIYAMA Sayuri
TSUBOI Eri
TANNE Kazuo
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | semaphorin3A / condyle / cartilage / chodrocytes / inflammation / arthritis / temporomandibular / TMD / 炎症 / 軟骨破壊 / MMP / 軟骨細胞 / 機械的刺激 / 関節炎 / mechanical stress / 細胞・組織 / 歯学 / 再製医療 / 遺伝子 / 生理活性 |
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| Outline of Final Research Achievements |
Experiment 1: We examined mRNA expression levels using qPCR analysis. The addition of Sema3A significantly inhibited gene expression of inflammatory mediators. We also examined protein expression of IL-1β and MMP-13 under CTS for 24h using Western blot analysis. The addition of Sema3A significantly and dosedependently inhibited expression of IL-1β and MMP-13.To verify whether AKT, ERK, and NF-κB are activated by excessive loading, we measured the expression of p-AKT, p-ERK, and p-NF-κB in ATDC5 cells under CTS for 1h. The phosphorylation of AKT, ERK, and NF-κB was upregulated by CTS according to Western blot analysis and the phosphorylation of AKT, ERK, and NF-κB was slightly blocked by Sema3A.
Experiment 2:The in vivo experiments using rat TMD model is still ongoing in order to clarify the role of sema3A histologically for inflammation in cartilage.
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| Academic Significance and Societal Importance of the Research Achievements |
申請者らは、神経細胞の成長方向を規定する因子であるsemaphorin3Aの軟骨における機能に着目し検討を行った。軟骨細胞に機械的刺激を付与したときに生じる炎症関連因子の発現（IL1-β、TNFα、COX2、MMP3および13）はsemaphorin3A添加により有意に抑制された。この結果は進行性下顎頭吸収のような顎関節疾患の予防法へとつながる貴重な知見だと考える。
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