Title: Gene expression of primary human bronchial epithelial cells in response to coal dusts with different prevalence of coal workers' pneumoconiosis.
Authors: Hu, Wenwei; Zhang, Qi; Su, Wei Cheng; Feng, Zhaohui; Rom, William; Chen, Lung Chi; Tang, Moonshong; Huang, Xi
Published In J Toxicol Environ Health A, (2003 Jul 11)
Abstract: Striking regional differences in the prevalence of coal workers' pneumoconiosis (CWP) have been observed but not fully understood. This study investigated the early biological responses of primary lung cells to treatment with coal dusts from various seams. High-density oligoarray technology (GeneChip, Affymetrix, Santa Clara, CA) was used to compile gene expression profiles of primary human bronchial epithelial cells to low concentrations (2 microg/cm(2)) of coals for 6 h or 24 h of treatment. Data showed that a total of 1050 out of 12,000 genes on the chip were altered by 2 coal dusts. The coal from the Pennsylvania (PA) coal-mine region with a high prevalence of CWP altered 908 genes, many more than the coal from Utah (UT) with a low prevalence of CWP, which affected 356 genes. Many genes decreased their expression levels in response to the PA coal at 6 h and/or 24 h of treatment. For example, transferrin receptor, a gene known to control cellular iron uptake, was downregulated in the cells treated with the iron-containing PA coal in order to protect cells from iron overload. The UT coal without bioavailable iron had no such effect. The downregulation patterns of genes were confirmed by reverse-transcription polymerase chain reaction (RT-PCR). This study is one of the first in profiling gene expressions of primary bronchial epithelial cells treated with coals from various seams, which may set stages for future studies on specific genes.
PubMed ID: 12851122
MeSH Terms: Cell Culture Techniques; Coal/adverse effects*; Down-Regulation; Epithelial Cells/physiology*; Gene Expression Regulation*; Humans; Inhalation Exposure*; Lung/cytology; Lung/pathology; Occupational Exposure*; Pneumoconiosis/epidemiology; Pneumoconiosis/etiology*; Pneumoconiosis/genetics; Prevalence; Reverse Transcriptase Polymerase Chain Reaction