| Project/Area Number |
06454428
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Orthopaedic surgery
|
|---|
| Research Institution | Osaka University |
|---|
Principal Investigator |
HAYASHIDA Kenji (1996-1997) Osaka University Medical School, Assistant Professor, 医学部, 助手 (50273686)
木村 友厚 (1994-1995) 大阪大学, 医学部, 講師 (80167379)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
YASUI Natsuo Osaka University Medical School, Associate Professor, 医学部, 助教授 (00157984)
OCHI Takahiro Osaka University Medical School, Professor, 医学部, 教授 (80112035)
大脇 肇 大阪大学, 医学部, 助手 (60223872)
|
|---|
| Project Period (FY) |
1994 – 1996
|
| Project Status |
Completed (Fiscal Year 1997)
|
| Budget Amount *help |
¥6,900,000 (Direct Cost: ¥6,900,000)
Fiscal Year 1996: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1995: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1994: ¥3,400,000 (Direct Cost: ¥3,400,000)
|
|---|
| Keywords | collagen / cartilage / gene defect / transgenic mice / chondro dysplasia / 遺伝子 |
|---|
| Research Abstract |
We focused on the following three topics during the period of this Grant-in-Aid for Scientific Research.
1. Analysis of the regulation mechanism in alpha2 (XI) collagen gene expression. We screened mouse genomic library by plaque hybridization. Probe was the cDNA fragment of mouse alpha2(XI) collagen which we had cloned previously. We analyzed the promoter elements of this gene by producing transgenic mouse. We found that twe different elements within this promoter govern both time dependent and position dependent cartilage development during embryonic stage.
2. Analysis of type XI collagen chain expression in cartilaginous tumor in humans. We analyzed and demonstrated that transcripts of alpha1, alpha2, alpha3 chains of type XI collagen undergoes different splicing in cartilaginous tumor.
3. Analysis of type IX collagen transgenic mouse. The transgenic mice expressing abnormal type IX collagen gene showed degeneration in articular cartilage and intervertebral discs, indicating that molecular abnormalities in cartilage collagen may result in human diseases of joint or spine.
|
