Figure 2

M-CSF-stimulates SR-A expression by upregulating SR-A mRNA and protein synthesis which requires p38 MAPK activation. (A) MPM were incubated with or without M-CSF (25 ng/ml) for 10 min at 37°C. Cells were then lysed with MBST/OG buffer and phosphorylation of MAPK quantified by immunobloting. The results from a single experiment are shown and are representative of at least four separate experiments. (B) MPM were treated as indicated with specific inhibitors of p38 [SB203580 (10 μM)], JNK [SP600125 (20 μM)] or ERK1/2 [PD98059 (10 μM)] for 20 minutes at 37°C. Cells were then treated with or without M-CSF (25 ng/ml) for 24 hrs at 37°C and SR-A protein quantified by immunoblotting. Data represent the mean ± SEM from at least three independent experiments.* denotes significant difference (p < 0.05) from untreated control value (ANOVA with Dunnett's multiple comparison). (C) MPM were treated with specific inhibitors of p38 [SB203580 (10 μM)], JNK [SP600125 (20 μM)] or ERK1/2 [PD98059 (10 μM)] for 20 minutes at 37°C, and then incubated with M-CSF (25 ng/ml) for 24 hrs. SR-A-specific macrophage association was quantified by flow cytometry as described in Materials and Methods. Data represent the mean ± SEM from at least three separate experiments. * denotes significant difference (p < 0.05) from M-CSF treated control value (ANOVA with Dunnett's multiple comparison).