SWCNT exposure of alveolar epithelial cells and macrophages induced OPN and TGF-beta1 response
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2011/03/01
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Description:Exposure of the lung to carbonaceous nanoparticles: single walled carbon nanotubes (SWCNT) leads to the development of pulmonary fibrosis (PF) and induction of a network of pro-fibrotic/pro-inflammatory cytokines including TGF-beta1 and osteopontin (OPN). TGF-beta1 is involved in fibrotic remodeling including fibroblast differentiation and enhanced deposition of collagen in the extracellular matrix. As part of the inflammatory cascade, OPN acts as a chemoattractant to guide polymorphonuclear neutrophils (PMN) and macrophages (M Phi) to the area of insult/injury and is also involved in collagen deposition. Potential interactions between OPN and TGF-beta1 have not been investigated even though both cytokines have been shown to be upregulated in response to SWCNT. We hypothesize that OPN increase in response to SWCNT potentiate TGF-beta1 production in lung cells. To test our hypothesis two cell types, alveolar epithelial cells (MLE-15) and RAW 264.7 M Phi were treated with SWCNT (6 mu g/cm2 - 48 mu g/cm2, for 24 hours). Exposure of the cells to SWCNT resulted in significantly enhanced OPN released found in the incubation medium (39.1% for MLE-15 and 38.6% for RAW 264.7 M Phi vs. respective controls). Using an OPN antibody we demonstrated an inhibition of OPN production in response to SWCNT. Further studies are needed to evaluate interplay between OPN and TGF-beta1 and their role in SWCNT induced pulmonary fibrosis. [Description provided by NIOSH]
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ISSN:1096-6080
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Volume:120
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NIOSHTIC Number:nn:20038618
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Citation:Toxicologist 2011 Mar; 120(Suppl 2):463
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Federal Fiscal Year:2011
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Peer Reviewed:False
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Source Full Name:The Toxicologist. Society of Toxicology 50th Annual Meeting and ToxExpo, March 6-10, 2011, Washington, DC
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Supplement:2
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Main Document Checksum:urn:sha-512:4ac337418b5151b7c7362fb84a6ff767b6ae4f374187b29a895613d5661b02a43b179cc86e5de6b08566caec7ff3d7bfdc736d821c1533c8aa23e1dcb344a346
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