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DIFFERENTIAL GENE EXPRESSION PROFILES IN RAT TRACHAEL EPITHELIAL (RTE) CELLS IN RESPONSE TO COMBUSTION-SOURCE PARTICULATE MATTER (PM) AND VANADIUM (V) A PRIMARY METAL CONSTITUENT
Citation:
Nadadur, S. S., J A. Dye, AND D L. Costa. DIFFERENTIAL GENE EXPRESSION PROFILES IN RAT TRACHAEL EPITHELIAL (RTE) CELLS IN RESPONSE TO COMBUSTION-SOURCE PARTICULATE MATTER (PM) AND VANADIUM (V) A PRIMARY METAL CONSTITUENT. Presented at Society of Toxicology, Baltimore, MD, March 21-25, 2004.
Description:
Differential gene expression profiles in rat tracheal epithelial (RTE) cells in response to combustion-source particulate matter (PM) and vanadium (V) a primary metal constituent
Srikanth S. Nadadur, Janice A. Dye and Daniel L. Costa, US EPA, ORD, NHEERL (ETD, Pulmonary Toxicology Branch), Research Triangle Park, NC 27711.
Epidemiological studies have associated increased mortality and morbidity in people with cardiopulmonary diseases with increased levels of ambient particulate matter (PM). The molecular basis for the cardiopulmonary health effects of PM and its constituents are still largely unknown. As one of our efforts to identify key target cell populations within the cardiopulmonary system, in the present study, we examined the acute cell responses in a primary airway epithelial cultures using microarray analysis. The RTE cells were exposed to an aqueous extract of model combustion PM, residual oil fly ash (ROFA, 50 mg/ml) and one of its major metal constituents, vanadium (V, at 1 and 7.7 mM), or saline for 25 min. Atlas Rat 4K plastic microarray (Clontech, Palo Alto, CA) was hybridized with 33P-labeled cDNA probe generated from poly A+ RNA isolated from the saline, ROFA or V exposed RTE cells. The spot intensities on the microarray were analyzed using AtlasImage 2.7 software (Clontech, Palo Alto, CA). Gene expression data was analyzed using GeneSpring software (Silicon Genetics, Redwood City, CA). A minimum three-fold exposure specific differential expression was observed in 870 genes. Of these, 479 genes were found up regulated. ROFA induced up regulation was seen in 139 genes, while 82 genes were suppressed. Induction of 293 genes by 1mM of V and suppression of an equivalent number of genes by 7.7 mM of V suggested concentration dependent transcriptional activation. Differential induction of chemokines, colony stimulating factor-2 by ROFA and V, and induction of colony stimulating factor-3 and CXC chemokine LIX by V only suggest possible roles for these genes in the initiation and progression of epithelial cell injury. (This abstract does not reflect US EPA policy).