1994 Fiscal Year Final Research Report Summary
Gene cloning of a novel cytokine inducing ICAM-1
| Project/Area Number |
04670382
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
内科学一般
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
MIYASAKA Nobuyuki Tokyo Medical and Dental University, Medical Research Institute, Professor, 難治疾患研究所, 教授 (30157622)
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| Project Period (FY) |
1992 – 1994
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| Keywords | adhesion molecule / matastasis / vascular endothelial cells |
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| Research Abstract |
The interaction between lymphoma cells and vascular endothelial cells (EC) is the first critical step in the ivasion of lymphoma cells. We found that invasive human CCRF-CEM T lymphoma cells (CEM) released a factor that upregulates the expression of adhesion molecules on vascular EC.The supernatant of CEM (CEM-SUP) increased the expression of both ICAM-1 and ELAM-1 in time- and dose-dependent manners as shown by cell enzyme-linked immunoadsobent assay (ELISA). In contrast, the induction of VCAM-1 on EC with CEM-SUP was relatively weak. No reactivity for interleukin-lalpha, interleukin-1 beta, interferon-gamma, or tumor necrosis factor alpha, which are known to augment ICAM-1 expression, was detected in CEM-SUP by ELISA.In reverse transcriptase polymerase chain reaction (RT-PCR) assay, CEM expressed a minimum amount of tumor necrosis factor alpha mRNA but absolutely no interleukin 1 beta and interferon gamma mRNA.In addition, anttibodies to cytokines did not inhibit the upregulatory effect of CEM-SUP.Semipurified CEM-SUP further increased the cellular binding between CEM cells and EC in vitro. This factor was stabel to heat (65ﾟC,30 min) and labile to acid (pH2). Gel filtration and chromatofocusing estimated its molecular weight at 50 with an isoelectric point of ph 7.2. Produciton of this factor might contribute the invasive charcter of cEM through upregulation of adhesion molecules on EC.
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