1996 Fiscal Year Final Research Report Summary
Molecular mechanisms of chronic inflammaroty proliferative disease
| Project/Area Number |
06404023
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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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 | Osaka University |
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Principal Investigator |
HIRANO Toshio Osaka University, Medical School, Professor, 医学部, 教授 (40136718)
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| Co-Investigator(Kenkyū-buntansha) |
ISHIHARA Katsuhito Osaka University, Medical School, Assistant Professor, 医学部, 助手 (10263245)
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| Project Period (FY) |
1994 – 1996
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| Keywords | rheumatoid arthritis / bone marrow stromal cell / BST-1 / cytokine / IL-6 / signal transduction / gene expression / inflammation |
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| Research Abstract |
We have proposed a disease category which should be called as chronic inflammatory proliferative disease (CIPD). CIPD shows 1) chronic inflammation, 2) chronic proliferation of pathogenic cells, 3) involvement of immune response and 4) deregulated expression of multiple genes. We have analyzed gene products expressed in rheumatoid arthritis (RA), one of typical CIPD.We isolated novel cell surface molecules, BST-1 and BST-2 from RA-derived bone marrow stromal cells. We showed that certain severe RA patients have a large amount of soluble BST-1 in sera. Our trial to identify the molecular mechanisms which are involved in the deregulated expression of IL-6 in RA has not been successful, but we showed that human parvovirus product can induce IL-6 gene expression through NF-kappaB.We also elucidated the molecular mechanisms of interleukin 6, another molecule involved in CIPD.Our study showed that JAK-STAT signal transduction pathway plays critical roles in cell growth and survival.
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