Inhibition of AhR activity augments CSE-induced COX-2 protein expression.

<p>(A) There was a slight but detectible increase in COX-2 in the AhR^+/− fibroblasts treated with CH-223191 alone (panel <i>ii</i>, arrowheads). When cells were exposed to both CSE and CH-223191, there was a strong induction of COX-2 (panel <i>iv</i>, arrows). Magnification = 40×. (B) There was a significant increase in the percentage of COX-2-positive cells in response to CH-223191 with or without CSE. Results are expressed as the mean ± SEM for 5 randomly-selected fields per triplicate experiment (**p<0.01). (C) There was a significant induction (fold-change: 4.93±2.4) in COX-2 protein expression when AhR-expressing cells were exposed to CH-223191 and 1% CSE compared to exposure to DMSO alone. Results are expressed as the mean ± SEM of 3 independent experiments. Representative western blot is shown. (D) Human lung fibroblasts- There was a slight but detectable increase in CSE-exposed human lung fibroblasts (panel <i>iii</i>). When cells were exposed to both 1% CSE and CH-223191, there was a stronger induction of COX-2 (panel <i>iv</i>, arrows). Magnification = 40×. (E) There was a significant increase in the percentage of COX-2-positive human lung fibroblasts in response to CH-223191 and exposed to CSE. Results are expressed as the mean ± SEM for 5 randomly-selected fields per triplicate experiment (**p<0.01; ***p<0.001). (F) There was a significant induction in COX-2 protein expression in human lung fibroblasts exposed to 1% CSE in conjunction with CH-223191 (3.1±0.84; *p<0.05 compared to both media control and 1% CSE alone). Representative western blot is shown. Results are expressed as the mean ± SEM of experiments utilizing fibroblasts from three different individuals.