| Project/Area Number |
12470376
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Plastic surgery
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| Research Institution | Tokyo Medical & Dental University |
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Principal Investigator |
HATA Yuiro Tokyo Medical & Dental Univ., Faculty of Medicine, Professor, 大学院・医歯学総合研究科, 教授 (90164839)
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| Co-Investigator(Kenkyū-buntansha) |
HIRASHIMA Mitsuomi Kagawa Medical University, Faculty of Medicine, Professor, 医学部, 教授 (70109700)
SATOH Takahiro Tokyo Medical & Dental Univ., Faculty of Medicine, Assistant Professor, 大学院・医歯学総合研究科, 講師 (30235361)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥14,800,000 (Direct Cost: ¥14,800,000)
Fiscal Year 2001: ¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2000: ¥11,800,000 (Direct Cost: ¥11,800,000)
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| Keywords | galectin / ecalectin / keloid / hyperplastic scar / fibroblast / cytokine |
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| Research Abstract |
Keloid and hyperplastic scar formation during wound healing is supposed to be important for surgical fields. Nevertheless the significance of involvement of various cytokines in those conditions, our understanding is not sufficient yet. Recently, we succeeded to clone an eosinophil chemoattractant, ecalectin, which is produced and released from antigen-stimulated T cells. We further found that ecalectin belongs to galectin family and galectin-9 is ecalectin. Galectin-9 may also functions as an adhesive molecule in those skin lesions similar to other galectins. The purpose of this project is to analyze the function and dynamics of galectin-9 in keloid and hyperplastic scar for prediction of those diseases.
We prepared most of galectin recombinant proteins and rabbit antibodies against respective galectin including galectin-9. For establishment of sensitive quantitative measurement of galectin-9, we prepared goat anti-galectin-9 antibody, and are preparing mouse monoclonal antibodies against galectin-9. Now, we are establishing ELISA methods for this purpose.
During this project, we found that galectin-9 expression is more up-regulated in the skin lesions of the above pathological conditions than normal skin. Furthermore, keratinocytes and fibroblasts expressed evident galectin-9. Therefore, regulation of galectin-9 expression was studied. So far, we found that interferon-ganmma up-regulated galectin-9 expression in flbroblasts, and expressed galectin-9 may play a crucial role in the selective eosinophil adhesion to the fibroblasts. Such adhesion was suppressed by lactose and anti-galectin-9 antibody, suggesting direct involvement of galectin-9 in the adhesion via its lectin nature. Furthermore, galectin-9 expression of not only fibroblasts but also keratinocytes was found to be up-regulated or suppressed by various cytokines.
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