Gene therapy for osteochondral defect
| Project/Area Number |
13671516
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Orthopaedic surgery
|
|---|
| Research Institution | Ehime University |
|---|
Principal Investigator |
WATANABE Shohei Ehime University, University Hospital, Assistant Professor, 医学部附属病院, 講師 (80253300)
|
|---|
| Project Period (FY) |
2001 – 2002
|
| Project Status |
Completed (Fiscal Year 2002)
|
| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2001: ¥2,300,000 (Direct Cost: ¥2,300,000)
|
|---|
| Keywords | Gene therapy / Osteochondral injury / Adenovirus / FGF2 / IL-4 / Plasmid / IL4 |
|---|
| Research Abstract |
1. To determine the therapeutic effect of FGF-2 mediated adenovirus vector on the osteochondral injury of the knee joints, AdCAsFGF-2 was administrated to the male Wister rats intravenously, in which knee joint osteochondral defect model was made by drilling with a surge-airtome. It was observed that cartilage repair was seen in the knee joints of rats with which were administrated AdCAsFGF-2 compared with rats injected with AxCAEGFP, control virus. Although there was the problem to induce the inflammation by AdCAsFGF-2, it seemed that local administration with vecotrs could be a therapeutic method for osteochondral injury.
2. To examine the effect of IL-4 on matrix synthesis in chondrocytes under excessive mechanical stress in vitro. Mechanical stress for 16 hours significantly decreased levels of mRNA for both AGG and CII (p <0.01), but rat IL-4 at doses of 1 or 10 ng/ml recovered these levels (p <0.05). These findings suggested that IL-4 might prevent articular cartilage from damage caused by mechanical stress and therefore could be a useful therapeutic agent for treatment of arthritic disorders.
3. Fibronectin is one of the major extracellular matrix components in synovium, and it plays a central role in cell-cell and cell-matrix interactions through ligation of cell surface integrins. In the present study, a 15 amino acid peptide derived from the carboxy-terminal 33-kD cell and heparin-binding domain of fibronectin (FN-C/H-II) suppressed established arthritis in mice, associated with reduced infiltration of inflammatory cells into the joint.
|
Report
(3 results)
Research Products
(3 results)
