| Project/Area Number |
16591496
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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 | The University of Tokushima |
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Principal Investigator |
MATSUI Yoshito The University of Tokushima, Institute of Health Biosciences, Lecturer, 大学院・ヘルスバイオサイエンス研究部, 助手 (80335348)
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| Co-Investigator(Kenkyū-buntansha) |
YASUI Natsuo The University of Tokushima, Institute of Health Biosciences, Professor, 大学院・ヘルスバイオサイエンス研究部, 教授 (00157984)
KATOH Shinsuke The University of Tokushima, Institute of Health Biosciences, Associate Professor, 大学院・ヘルスバイオサイエンス研究部, 助教授 (30243687)
NIKAWA Takeshi The University of Tokushima, Institute of Health Biosciences, Associate Professor, 大学院・ヘルスバイオサイエンス研究部, 助教授 (20263824)
HIGASHINO Kosaku The University of Tokushima, University Medical and Dental Hospital, Lecturer, 医学部・歯学部附属病院, 助手 (80380129)
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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 |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2005: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2004: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | type IX collagen / polymorphism / spondylolisthesis / Lumbar disc herniation / MRI / matrix / tryptophan / multiple epiphyseal dysplasia / 椎間板 / 変性 / 血管新生 / VEGF |
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| Research Abstract |
We analyzed the type IX collagen gene polymorphism, which introduces tryptophan residue into the triple helical region of the molecule, in relation with lumbar disc degeneration.
The allele frequency of the polymorphism was 21% among the Japanese healthy controls (Clin Rheumatol in press). We demonstrated that the polymorphism was associated with lumbar spondylolisthesis (J Bone Joint Surg Br 2004). We also found that the polymorphism was significantly related to severe disc degeneration, evidenced by MRI, among the young generation of the Japanese patients with lumbar disc herniation (manuscript in preparation). Protein analysis of the removed disc tissues from the patients revealed that the type IX collagen content was very low (manuscript in preparation), indicating that the destruction of this molecule is involved in the development of early-onset disc matrix degeneration. Lastly, we identified a Japanese family with multiple epiphyseal dysplasia caused by the type IX collagen gene mutation (Clin Rheumatol in press), showing a possible predisposition to lumbar spondylolisthesis (manuscript in preparation).
In summary, our results imply that the genetic variation of collagen IX is a risk factor for lumbar disc degeneration in the Japanese population.
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