| Project/Area Number |
12672034
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Periodontal dentistry
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| Research Institution | Osaka University |
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Principal Investigator |
SHIMABUKURO Yoshio Dental hospital, Department of periodontology, Osaka University, assistant professor, 歯学部・附属病院, 講師 (50231361)
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| Co-Investigator(Kenkyū-buntansha) |
TAKAYAMA Shinichi Graduate School of Dentistry, Department of periodontology, Osaka University, Research associate, 大学院・歯学研究科, 助手 (00314386)
SAHO Teruyuki Dental hospital, Department of periodontology, Osaka University, Research associate, 歯学部・附属病院, 助手 (10263295)
MURAKAMI Shinya Graduate School of Dentistryn, Department of periodontology, Osaka University, Professor, 大学院・歯学研究科, 教授 (70239490)
岡田 宏 大阪大学, 大学院・歯学研究科, 教授 (40038865)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2001: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2000: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Hyaluronan / Hyalurona synthase / Hyaluronidase / depolymeraized hyaluronan / nitric oxide / adenosine / HAS / サイトカイン / iNOS |
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| Research Abstract |
We analyzed the effects of inflammatory mediator on hyaluronan synthesis by human gingival fibroblasts. IL-1β and TGFβ increased the hyaluronan productions and the proportion of high molecular weight of hyaluronan. TGFβ-activated gingival fibroblast produced the highest polymerization followed by IL-1 β-stimulated gingival fibroblasts which were more than unstimulated fibroblasts.
This result was consistent with the observation that IL-1β up-regulated the HAS1, 2, and 3 mRNA, TGFβ enhanced only HAS1mRNA, since HAS1 is reported to produce high molecular weight of hyaluronan.
Hyal 1, 2, and 3 were not altered by both IL-1β and TGFβ.
Activation of human gingival epithelial cells with both IL-1β and TNFa or 2-CADO, adenosine receptor agonist, resulted in the elevation of iNOS mRNA and NO_2 and NO_3, stable NO derivatives. Since it is reported that NO and peroxynitrite, its metabolite, depolymerized high molecular weight hyaluronan to low molecular size, it is speculated that low molecular weight of hyaluronan was accumulated during inflammatory lesion.
In turn, it seems that depolymerized hyaluronan which was recently recognized as a proimflammatory mediator deteriorate the inflammation.
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