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Use of Transgenic Luciferase Reporter Mice To Determine Activation of Transcription Factors and Gene Expression by Fibrogenic Particles*

Andrea K. Hubbard, PhD; Cynthia R. Timblin, PhD; Mercedes Rincon, PhD; Brooke T. Mossman, PhD
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*From the Department of Pharmaceutical Sciences (Dr. Hubbard), University of Connecticut, Storrs, CT; and the Departments of Pathology (Drs. Timblin and Mossman) and Medicine (Dr. Rincon), University of Vermont, Burlington, VT.

Correspondence to: Brooke T. Mossman, PhD, Department of Pathology, A-145 Medical Alumni Building, University of Vermont College of Medicine, Burlington, VT 05405; e-mail: bmossman@zoo.uvm.edu



Chest. 2001;120(1_suppl):S24-S25. doi:10.1378/chest.120.1_suppl.S24
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Exposure to silica or asbestos elicits a striking inflammatory response that is characterized by the influx of inflammatory cells, increased expression of inflammatory cytokines, cell injury, and compensatory cell proliferation.1 The regulation of these events may be dependent on the activation of transcription factors such as nuclear factor-κB (NF-κB) and/or activator protein-1 (AP-1) since the promoter regions of many genes involved in inflammation, proliferation, and/or apoptosis are known to contain binding sites for these transcription factors.23 Previous work from this laboratory has demonstrated increased AP-1 binding to DNA and AP-1-dependent gene transcription in mesothelial cells and tracheal epithelial cells after exposure to asbestos in vitro.5 We and others67 also have shown that asbestos causes NF-κB activation in these cell types in vitro and in an inhalation model of asbestosis. However, whether silica causes transcriptional activation of NF-κB and AP-1-dependent gene expression in the lung after exposures in vivo is unclear.

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