1998 Fiscal Year Final Research Report Summary
Regulation mechanism of nsulin-like growth factor-binding proteins producion in osteoarthritis.
| Project/Area Number |
09671503
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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 | Nagasaki University |
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Principal Investigator |
MATSUMOTO Tomoko Nagasaki University, School of Medicine Hospital, Assistant, 医学部附属病院, 助手 (30239107)
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| Co-Investigator(Kenkyū-buntansha) |
YAMASHITA Shunichi Nagasaki University, School of Medicine, Professor, 医学部, 教授 (30200679)
ENOMOTO Hiroshi Nagasaki University, School of Medicine, Assistant, 医学部, 助手 (90284679)
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| Project Period (FY) |
1997 – 1998
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| Keywords | Osteoarthritis / IGF-bimding protein / Isulin-like growth factor-1 |
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| Research Abstract |
Thc destruction of cartilage tissue causes functional disability in osteoarthritis. The repair of cartilage tissue are supposed to be disturbed in this disease. Insulin-like growth factor (IGF) is an anabolic factor for chondrocytes and is regulated by binding proteins (IGPBPs). We assumed that the effect of IGF-I on chondrocytes are disturbed in osteoarthritis. So we tried to study the IGFBPs produced by human chondrocytes, which may regulate IGE action. Employing Western-ligand blotting (WLB) and immunoprecipitation, immortalized humah chondrocytes were found to secrete IGFBP-2, -3, -4 and -5. Treatment of cells with IGF-I resulted in a dose-dependent increase of IGFBP-5. The IGFBPs associated with cell membrane were examined by affinity cross-linking method, showing the IGFBP-3 and -5 as well as type 1 LGF and type 2 [GE receptor. To clarify the changes of IGFBPs in osteoarthritis, interleukin-1b is added to the culture medium. Unfortunately, there was no difference between them, with /without interleukin-1. We should further study the regulation mechanism of IGEBP production in osteoarthritis by using human cartilage tissue obtained by operated sample.
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