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Stress genes as biomarkers of mineral dust exposure.
Department of Pathology, University of Vermont, Burlington, Vermont 1997 Dec; :1-7
An evaluation was conducted of in-vitro and in-vivo models of asbestos (1332214) or silica (14808607) exposure for changes in hsp70, grp78, gadd45, gadd153 steady state mRNA and to relate asbestos or silica induced changes in-vitro to other oxidant stress inducing agents. Characterization of the patterns of gene expression and the functional roles of the encoded proteins provide valuable insights into how a cell responds to injury and how injury can result in the development of disease. The findings showed that crocidolite (12001284) asbestos and other oxidant stress inducing agents elicit different patterns of GRP78, HSP72/73, cJun and MnSOD protein expression. Functional studies examining the role of cJun in the response of epithelial cells to crocidolite asbestos induced injury have demonstrated that asbestos directly activates AP-1- dependent gene expression. Over expression of cJun in tracheal epithelial cells results in increased cell proliferation and cellular transformation, indicating that asbestos induced changes in gene expression can result in changes in cell phenotype that are significant in disease development. The authors indicate that their findings support increasing evidence indicating that environmental agents causing oxidative injury to lung epithelium elicit different patterns of stress protein responses.
NIOSH-Grant; Cancer; Pulmonary-system-disorders; Protein-chemistry; Asbestos-fibers; Fibrous-bodies; Lung-irritants; Dust-exposure; Mineral-dusts
Pathology University of Vermont Medical Alumni Bldg Burlington, VT 05405
1332-21-4; 14808-60-7; 12001-28-4
Final Grant Report
NTIS Accession No.
Department of Pathology, University of Vermont, Burlington, Vermont
University of Vermont & St Agric College, Burlington, Vermont
Page last reviewed: March 11, 2019
Content source: National Institute for Occupational Safety and Health Education and Information Division