| Project/Area Number |
08671628
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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 | HOKKAIDO UNIVERSITY |
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Principal Investigator |
SUZUKI Koji Hokkaido Univ., Med.Hospital., Instructor, 医学部・附属病院, 助手 (90235945)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUNO Takeo Asahikawa Medical College., School of Medicine, Professor, 医学部, 教授 (10165847)
NISHIHIRA Jun Hokkaido Univ., School of Medicine, Lecturer, 医学部, 講師 (30189302)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1996: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | loosening / soluble factors / macrophage migration inhibitory factor / foreign body reaction / osteoblast / cell proliferation / 人工関節のゆるみ / Macrophage / 貧食 |
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| Research Abstract |
In bone tissues, the bone mass is strictly regulated by osteoblastic bone formation and osteoclastic bone resorption, i.e., coupling. Failure of this balance results in the pathologic state of bone. In the aged society where we have to deal with problems such as fractures due to osteoporosis etc., it is extremely important to understand and regulate the mechanism of bone metabolism.
An example of the pathologic bone resorption is the loosening of implant due to focal osteolysis after total hip arthroplasty (THA). This phenomenon, which is the major cause of poor long-term results of THA,has been speculated to arise from the foreign body reaction against polyethylene wear debris. We investigated the involvement of macrophage migration inhibitory factor (MIF) in this process. The results are as follows. 1) In the pseudosynovial tissues retrieved at revision THA surgery, macrophages that phagocytosed polyethylene wear debris were immunohistochemically positive for MIF.2) In in-vitro study with the use of murine macrophage cell line RAW264.7 and fluorescene-coated latex beads, macrophages released MIF into culture supernatants dose-dependently in response to the phagocytosis of the beads, which was accompanied by the up-regulation of MIF _mRNA.3) Pretreatment of the cells with rat-MIF (10mu g/ml) for 48hours promoted the cells to phagocytose 1.6-folds more beads compared with the control.
Apart from the role as a mediator of inflammation, MIF has recently been suggested to be involved in the cell proliferation. We investigated the expression of MIF in osteoblasts of highly proliferative stage. The results are as follows. 1) Immunohistochemistry showed that MIF was positive in the cytosol of both murine calvarial osteoblasts and MC3T3E1 cells. 2) The expression of MIf by these cells was shown by Western blot and RT-PCR.Taken together, the involvement of MIF in the proliferation of osteoblasts was suggested.
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