| Interferon-gamma suppresses PDGF production from THP-1 cells and blood monocyte-derived macrophages. | |
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MedLine Citation:
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PMID: 1445496 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Involvement of the immunological mechanisms in atherogenesis has recently been suggested by immunohistological detection of macrophages and T lymphocytes in atherosclerotic lesions. In the present study, we have investigated the regulatory effect of interferon-gamma (IFN-gamma), a cytokine secreted by activated T cells, on the production and secretion of platelet-derived growth factor (PDGF) from macrophages in culture. The human monocytic leukemia cell line, THP-1, was treated with phorbol 12-myristate 13-acetate (PMA) for 24 h to induce macrophage differentiation and PDGF production, and then various doses of recombinant human IFN-gamma (0-1000 I.U./ml) were added to the culture. After 48 h, the conditioned medium and the cells were harvested and analyzed for PDGF production. PDGF-dependent mitogenic activity in the conditioned medium, estimated by neutralization of mitogenic activity with anti-PDGF antibody, was suppressed by IFN-gamma treatment. Radioimmunoassays for PDGF also revealed a decrease in both PDGF-AA and -BB in the conditioned medium with IFN-gamma treatment, whereas neither total cell DNA as an indication of cell number nor overall protein synthesis based on [3H]leucine incorporation were decreased. Northern analysis of total RNA extracted from the cells demonstrated that IFN-gamma suppressed the level of PDGF mRNA. Analysis of mRNA degradation in the presence of actinomycin D demonstrated that the decrease in PDGF mRNA was not due to enhanced degradation of mRNA. A similar inhibitory effect of IFN-gamma on PDGF mRNA levels was also found in monocyte-derived macrophages cultured in the presence of granulocyte-macrophage colony stimulating factor. These results suggest that IFN-gamma modulates production and secretion of PDGF from macrophages and that the functions of macrophages in atherogenesis may be regulated by the cellular interactions between T cells and macrophages through the action of cytokines such as IFN-gamma. |
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Authors:
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C Kosaka; J Masuda; K Shimokado; K Zen; T Yokota; T Sasaguri; J Ogata |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Atherosclerosis Volume: 97 ISSN: 0021-9150 ISO Abbreviation: Atherosclerosis Publication Date: 1992 Nov |
Date Detail:
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Created Date: 1992-12-14 Completed Date: 1992-12-14 Revised Date: 2008-11-21 |
Medline Journal Info:
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Nlm Unique ID: 0242543 Medline TA: Atherosclerosis Country: NETHERLANDS |
Other Details:
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Languages: eng Pagination: 75-87 Citation Subset: IM |
Affiliation:
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National Cardiovascular Center Research Institute, Osaka, Japan. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cell Division Cells, Cultured Culture Media, Conditioned DNA / biosynthesis Fibroblasts / cytology, metabolism Gene Expression Humans Interferon-gamma / pharmacology* Leukemia, Monocytic, Acute / metabolism* Macrophages / metabolism* Mice Platelet-Derived Growth Factor / biosynthesis*, genetics RNA, Messenger / analysis Radioimmunoassay Tetradecanoylphorbol Acetate / pharmacology Tumor Cells, Cultured / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Culture Media, Conditioned; 0/Platelet-Derived Growth Factor; 0/RNA, Messenger; 16561-29-8/Tetradecanoylphorbol Acetate; 82115-62-6/Interferon-gamma; 9007-49-2/DNA |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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