Figure 2

p38 MAPK activation. A. To assess MAPK activation, C57BL/6 and NZW mice were exposed to acute CS, and sacrificed at 0 h, 0.25 h, 1 h, 3 h, 6 h, 12 h, and 24 h from the start of CS exposure. B-E. Phosphorylated and total levels of p38 MAPK, ERK, and JNK in the lungs were analyzed by western blotting, with β-actin as an indicator for equal protein loading. Phosphorylation of p38 MAPK in the lungs was confirmed in C57BL/6 mice, but not in NZW mice. Phosphorylation of ERK and SAPK/JNK was noted in both strains in response to CS exposure. Western blots are representative of three independent experiments evaluating murine lungs at 1 hr after the start of acute CS exposure (C, D, E). The intensities of the electrophoretic bands were quantified and expressed as p-MAPK/t-MAPK. p-MAPK, phosphorylated-MAPK; t-MAPK, total MAPK. * p < 0.05 compared with corresponding non-smoke groups. †p < 0.05 compared with C57BL/6 smoke groups. n = 3 for each experimental set. F-I. Phosphorylated and total p38 MAPK following acute CS exposure were evaluated by immunohistochemistry. Acute CS exposure caused a marked increase in the number of phosphorylated p38-positive cells in the alveolar walls of C57BL/6 mice, but not NZW mice (F). Total numbers of p38-positive cells were not increased by acute CS exposure (G). Chronic CS exposure caused a marked increase in the numbers of both phosphorylated and total p38-positive cells in the alveolar walls of C57BL/6 mice, but not NZW mice (H, I). p-p38, phosphorylated-p38; t-p38, total p38. *p < 0.05 compared with corresponding non-smoke groups. †p < 0.05 compared with C57BL/6 smoke groups. n = 6 for each experimental set.