| Project/Area Number |
13470051
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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 |
Experimental pathology
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| Research Institution | Kagawa Medical University |
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Principal Investigator |
HIRASHIMA mitsuomi Kagawa Medical University, Faculty of Medicine, Professor, 医学部, 教授 (70109700)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAUCHI akira Kagawa Medical University, Faculty of Medicine, Visiting Professor, 医学部, 客員教授 (00291427)
NISHI nozomu Kagawa Medical University, Faculty of Medicine, Research Associate, 医学部, 助手 (10145047)
NAKAMURA takanori Kagawa Medical University, Faculty of Medicine, Professor, 医学部, 教授 (70183887)
SAITA naoki Kumamoto University Hospital, Research Associate, 医学部附属病院, 助手 (10274698)
OKADA hiroki Kagawa Medical University Hospital, Associate Professor, 医学部附属病院, 助教授 (00243775)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥14,400,000 (Direct Cost: ¥14,400,000)
Fiscal Year 2002: ¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 2001: ¥12,100,000 (Direct Cost: ¥12,100,000)
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| Keywords | Galectin-9 / Eosinophil / Immune Cell / Tumor cell / Galectin-binding Molecule / Chemotaxis / Cell Aggregation / Apoptosis |
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| Research Abstract |
1. Galectin-9 (Gal-9) is a unique eosinophil activation factor differing from other identified chemoattractants (J Immunol, 2002), and the linker peptide is found not to be involved in its function (Glycobiology, 2002). IFN induced up-regulation of Gal-9 in endothelial cells and fibroblasts, and the expressed Gal-9 on their surface is associated with selective adhesion of eosinophils (J Leukocyte Biol, 2002; J Immunol, 2002). We also found that Gal-9 induces aggregation and apoptosis of tumor cells such as melanoma and breast cancer, and higher Gal-9 expression is linked to better prognosis of those patients (Int J Cancer, 2002; 25^<th> San Antonio Breast Cancer Symposium). Thus, immunohistochemical analysis can be used for determining the prognosis of tumor patients, especially in remote metastasis.
2. Production and release of Ga-1-9 is induced by PMA in Jurkat T cell line, and an MMP is involved in the release (Glycobiology, 2002). We are continuing the study on the production and release of Gal-9 using mast cells and macrophages.
3. Apoptosis induced by Gal-9 is suppressed by the presence of lactose indicating that Gal-9 binding molecules (glycoprotein with beta-galactoside) is present on the surface. We found that Gal-9 induces apoptosis through calcium-calpain-caspase pathway (J Immunol, 2003 in press). Now, we have purified the candidates of Gal-9 binding molecule involving in Ga-9-induced apoptosis, and clarifying which molecule is the Gal-9 binding molecule for the apoptosis.
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