Diesel exhaust particles (
DEP) induce
pulmonary diseases including
asthma and
chronic bronchitis. Comprehensive evaluation is required to know the mechanisms underlying the effects of
air pollutants including
DEP on
lung diseases. Using a
cDNA microarray, we examined changes in gene expression in SV40T2 cells, a rat alveolar type II epithelial cell line, following exposure to an organic extract of
DEP. We identified candidate sensitive genes that were up- or down-regulated in response to
DEP. The
cDNA microarray analysis revealed that a 6-h exposure to the
DEP extract (30 microg/ml) increased (>2-fold) the expression of 51 genes associated with drug metabolism, antioxidation, cell cycle/proliferation/apoptosis, coagulation/fibrinolysis, and expressed sequence tags (ESTs), and decreased (<0.5-fold) that of 20 genes. In the present study,
heme oxygenase (HO)-1, an antioxidative
enzyme, showed the maximum increase in gene expression; and type II
transglutaminase (TGM-2), a regulator of coagulation, showed the most prominent decrease among the genes. We confirmed the change in the HO-1
protein level by Western blot analysis and that in the
enzyme activity of TGM-2. The organic extract of
DEP increased the expression of HO-1
protein and decreased the
enzyme activity of TGM-2. Furthermore, these effects of
DEP on either HO-1 or TGM-2 were reduced by
N-acetyl-l-cysteine (NAC), thus suggesting that oxidative stress caused by this organic fraction of
DEP may have induced these cellular responses. Therefore, an increase in HO-1 and a decrease in TGM-2 might be good markers of the biological response to organic compounds of airborne particulate substances.