2005 Fiscal Year Final Research Report Summary
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)
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| Project Period (FY) |
2004 – 2005
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| Keywords | positive feedback Loop / interbertebral disc herniation / pain mechanism / interleukin-1β |
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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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