| Project/Area Number |
17K16685
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Orthopaedic surgery
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| Research Institution | University of Yamanashi |
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Principal Investigator |
OHBA Tetsuro 山梨大学, 大学院総合研究部, 助教 (70456490)
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 腰痛 / 炎症 / マスト細胞 / 椎間板 / マストcell トリプターゼ / PAR-2 / 椎間板変性 / 肥満細胞 / 炎症性サイトカイン |
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| Outline of Final Research Achievements |
When the intervertebral disc collected from the mouse caudal vertebrae was stimulated with mast cell tryptase, the culture supernatant expressed inflammatory cytokines such as TSLP and MCP-1. This expression was independent of the concentration of mast cell tryptase and was dependent on the time of stimulation. Next, when cultured with administration of an inhibitor of PAR-2 signal simultaneously with mast cell tryptase, expression of inflammatory cytokines was not observed. Mast cell tryptase stimulation reduced the expression of the cartilage matrix of the intervertebral disc.
From the above, it has been suggested that mast cells induce expression of inflammatory cytokines via tryptase and PAR-2 signals, and are further involved in intervertebral disc degeneration by reducing the expression of cartilage matrix.
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| Academic Significance and Societal Importance of the Research Achievements |
椎間板に局在するマスト細胞がMCTによりPAR-2シグナルを活性化し、椎間板からのサイトカイン発現を誘導することが変性や腰痛に関与する可能性がある。PAR-2はすでに多分野で疼痛の治療標的分子として研究が進んでおり、臨床への応用が大いに期待できる。腰痛に対する新規分子標的の発見は、高齢化の進む我が国において意義が大きい。
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