2004 Fiscal Year Final Research Report Summary
Analysis of causative gene for lumbar disc disease and investigation of molecular mechanism for interverteral disc degeneration
| Project/Area Number |
14571364
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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 | Toyama Medical and Pharmaceutical University |
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Principal Investigator |
KAWAGUCHI Yoshiharu Toyama Medical & Pharmaceutical University, Department of Orthopedic Surgery, Lecturer, 医学部, 助手 (00262527)
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| Co-Investigator(Kenkyū-buntansha) |
ISHIHARA Hirokazu Toyama Medical & Pharmaceutical University, Department of Orthopedic Surgery, Lecturer, 附属病院, 講師 (30242499)
OSADA Ryusuke Toyama Medical & Pharmaceutical University, Department of Orthopedic Surgery, Assistant Prof., 附属病院, 助手 (40293310)
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| Project Period (FY) |
2002 – 2004
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| Keywords | Lumbar disc herniation / Lumbar disc disease / Genetic polymorphism / Case-control study / Vitamin-D receptor gene / Aggrecan gene / IX collagen gene / PCR |
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| Research Abstract |
Lumbar disc diseases are common problems in the young population. Although the etiology is unknown, it has been suggested that a genetic factor contributes to the development of these diseases. Recently, some genetic polymorphisms have been found to be related. We have examined the association between several genetic polymorphisms and lumbar disc diseases. Our previous studies found that the shorter VNTR (variable number of tandem repeat) in Exon 12 of aggrecan gene and the Tt polymorphism in Exon 9 of vitamin D receptor gene (VDR gene) have the positive association with lumbar disc degeneration and disc herniation in an early age. We collected more than 800 samples in cooperation with The Institute of Physical and Chemical Research (RIKEN), Keio University and Kyoto prefectural Univerisity. We examined other candidate genes which were shown as causal genes in previous literatures and confirmed that there were no association in our samples. However, we found the positive association between the haplotype of COL9A2 and lumbar disc diseases. Further, we found that the gene X had a strong association. The gene X codes the structural component of joint cartilage and intervertebral disc. We also examined the mechanism how the gene becomes a causative factor in disc disease. The paper including these results will be published in some scientific journal soon.
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