Investigation into a pain mechanism of Human Intervertebral disc herniation.
| Project/Area Number |
16591517
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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 |
Orthopaedic surgery
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| Research Institution | Kurume University |
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Principal Investigator |
PARK Jin Soo Kurume University, School of Medicine, Assistant, 医学部, 助手 (10368938)
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| Co-Investigator(Kenkyū-buntansha) |
NAGATA Kensei Kurume University, Professor, 医学部, 教授 (50140687)
TSURU Michiyo Kurume University, Biotechnology Statistics Center, Researcher, バイオ統計センター, 研究員 (90368887)
SATO Kimiaki Kurume University, Assistant Professor, 医学部, 助教授 (90268912)
津留 美智代 久留米大学, バイオ統計センター, 研究員 (80322600)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2005: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2004: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | positive feedback Loop / interbertebral disc herniation / pain mechanism / interleukin-1β / positive feedback loop / サイトカイン |
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| Research Abstract |
Object. IL-1β induces neurological symptoms in intervertebral disc herniation (IDH). Recently, the existence of a positive feedback loop of IL-1β which encourages an inflammatory reaction or degeneration in the cells of tendon has been reported. We hypothesized that there is a positive feedback loop of IL-1β in the cells of IDH.
Methods. Human intervertebral disc specimens were harvested during surgery for lumbar disc herniation. The cells were stimulated in serum-free medium with or without exogenous IL-1β. The mRNA was extracted for RT-PCR and real-time PCR to quantify the mRNAs of endogenous IL-1β, IL-6, COX-2, and MMPs. Secondly, the cells were stimulated in serum-free medium with or without exogenous IL-1β, and then exogenous IL-1β was removed. After 2, 4, and 6 days, the medium was collected to measure the protein concentration of endogenous IL-1β by ELISA. The mRNA expressions of endogenous IL-1β, IL-6, COX-2, and MMPs were increased significantly depending on the concentration of exogenous IL-1β. The protein concentration of endogenous IL-1β was increased with time.
Conclusions. There was a positive feedback loop of IL-1β in the cells of IDH. Furthermore, the productions of IL-6, COX-2, MMP-1 and MMP-3 were upregulated as a result of the increasing concentration of IL-1β, in a positive feedback loop of IL-1β. We concluded this positive feedback loop of IL-1β upregulated the production of mediators and thus caused to stagnation of symptoms in IDH.
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Report
(3 results)
Research Products
(3 results)
