Project/Area Number |
02807172
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
Conservative dentistry
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Research Institution | Okayama University |
Principal Investigator |
NOMURA Yoshio Okayama University, Dental School, Associate Professor, 歯学部, 助教授 (50107075)
|
Co-Investigator(Kenkyū-buntansha) |
GOTO Hirouki Okayama University, Dental School, Assistat, 歯学部, 助手 (90205609)
SHIMIZU Hideki Okayama University, Dental School, Assistat, 歯学部, 助手 (70170983)
KINOSHITA Masahiko Okayama University, Dental School, Assistant Professor, 歯学部附属病院, 講師 (80161537)
|
Project Period (FY) |
1990 – 1991
|
Project Status |
Completed (Fiscal Year 1991)
|
Budget Amount *help |
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1991: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1990: ¥1,200,000 (Direct Cost: ¥1,200,000)
|
Keywords | Fibroblast / Interleukin 1beta / Tumor necrosis factor alpha / Interleukin 6 / Interleukin 8 / Ttansforming growth factor / Prostaglandin E_2 / Cytokine network / 歯肉線維芽細胞 / DNA合成 / コラ-ゲン合成 |
Research Abstract |
Fibroblasts are regarded as potential participants in the orchestration of inflammation via the production of inflammatory mediators. In addition, the metabolism of fibroblasts are effected various cytokines and growth factors. The purpose of this study was to evaluate the effects of interleukin 1beta(IL-1beta)on metabolism of human gingival fibroblasts(HGF)and to evaluate the effects of various growth factors on metabolism of human periodontal ligament(HPL)cells. The results were as follows ; l)IL-1beta inhibited the proliferation of HGF. 2)IL-1beta greatly stimulated PGE_2 production from HGF. 3)IL-1beta inhibited the collagen synthesis, while did not influence to no. ncollagenous protein synthesis. 4)Addition of indomethacin'reversed the inhibition of DNA and collagen synthesis caused by IL-1beta. 5)EGF, INS and TGF stimulated DNA synthesis in PDL cells. DNA synthesis was significantly enhanced by the combination of FGF and INS, FGF and TGF, EGF and INS, EGF and TGF. 6)INS and TGF stimulated collagen synthesis in PDL cells. 7)TGF was the only growth factor that enhanced the activity of ALPase in monolayer PDL cells. 8)With stimulating of either IL-1beta or TNFalpha, HGF expressed IL-6 and IL-8 RNA, secreted IL-6 and IL-8 in a dose dependent manner. 9)IL-6 secretion from HGF was partially supressed by PGE_2.10)Neutralization assay using a rabbit anti-recombina. nt human IL-8 antiserum inhibited the neutrophil chemotactic activity manifested by the cells to basal level. 11)HGF did not express IL-6 receptor MRNA. 12)In inflamed gingiva, HGF were stained with anti-IL-6 antibody. These results suggested that HGF and PDL cells may play an important role to control the inflammatory process of periodontal disease.
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