Cytokine and Pharmacological Regulation of Lung Fibroblast Proliferation
Public Domain
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1992/02/01
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Description:Our objective was to study the role of macrophage-derived cytokines in fibroblast proliferation. [3H] thymdine incorporation was shown to correlate well with fibroblast proliferation. In vitro treatment of alveolar macrophages with silica (150microg/ml) resulted in the production of an agent(s) which inhibits fibroblast proliferation. Indomethacin, a prostaglandin synthetase inhibitor, reversed this inhibition and unmasked a previously unseen competence factor(s). Further, the proliferative action of exogenous PDGF was reduced when fibroblasts were treated with supernate from silica-exposed macrophages, presumably due to the inhibitory action of prostaglandins. Silica-induced pulmonary fibrosis may result from decreased release of prostaglandins and/or increased release of proliferative factors from alveolar macrophages. Indeed, macrophages harvested 40 days after intratracheal instillation of silica (42mg/rat) produced an agent(s) which significantly stimulated [3H] thymidine incorporation by pulmonary fibroblasts. The antifibrotic drug, tetrandrine, inhibited [3H] thymidine incorporation and fibroblast proliferation in response to either serum or PDGF plus plasma. Thus, tetrandrine may be a useful probe to study fibrogenesis. (BOM-5431) [Description provided by NIOSH]
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ISSN:0731-9193
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Volume:12
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Issue:1
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NIOSHTIC Number:nn:20037144
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Citation:Toxicologist 1992 Feb; 12(1):390
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Federal Fiscal Year:1992
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Peer Reviewed:False
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Source Full Name:The Toxicologist. Society of Toxicology 31st Annual Meeting, February 23-27,1992, Seattle, Washingtion
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Main Document Checksum:urn:sha-512:93b99094af93dd78c08a2a012a60760b189a18a504b07df72d99624696e7640312ffc7d2703e36cf14779ef2dbc02361618627b09c4a57e52f84a9756c31f728
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