2017 Fiscal Year Final Research Report
the unravelling of the role of cathepsin in gingival overgrowth
| Project/Area Number |
15K11393
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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 |
Periodontology
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
中西 博 九州大学, 歯学研究院, 教授 (20155774)
西村 英紀 九州大学, 歯学研究院, 教授 (80208222)
岩下 未咲 九州大学, 大学病院, 助教 (80611326)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | 歯肉増殖症 |
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| Outline of Final Research Achievements |
We previously suggested complete loss of Cathepsin-L function promoted gingival overgrowth.SPOCK-1,belonging to proteoglycan family, is a specific inhibitor of CtsL. The aim of this study is to investigate the role of SPOCK-1 in DIGO.
Human gingival fibroblasts were collected from patients who underwent flap operations.The cells were stimulated with Phenytoin (PHE), Cyclosporin A (CsA) or Nifedipine (NFE). The mRNA and protein levels of SPOCK-1 were examined by quantitative real time PCR and western blotting. As in vivo study, Spock-1 transgenic mice and wild-type littermates were generated, grown, and sacrificed. Gingival appearance was observed by microscopy. The results indicated that PHE, CsA and NFD promoted the expression of SPOCK-1 both at mRNA and protein level. The gingiva of Spock-1 transgenic mice exhibited different degree of fibrosis.SPOCK-1 upregulation was common among the three drug used, which may indicate the importance of SPOCK-1 in the pathophysiology of DIGO.
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| Free Research Field |
歯周病学
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