Fig. 8: Regulation of MMP-9 expression in peritoneal macrophages by CCL3 and its receptors.
a The effects of CCL3 on Mmp9 expression in WT macrophages stimulated by PMA for 24 h (n = 4 independent experiments). **P < 0.01, *P < 0.05, vs. no stimulation; ##P < 0.01, #P < 0.05, vs. PMA only. b The effects of CCL3 on PMA-induced Mmp9 expression in peritoneal macrophages obtained from WT, Ccr1−/−, and Ccr5−/− mice (n = 4 independent experiments). **P < 0.01, vs. no stimulation; ##P < 0.01, #P < 0.05, vs. PMA only. c Western blotting analyses on the expression of ERK, p-ERK, p38, p-p38, JNK, p-JNK, and GAPDH in WT macrophages stimulated by PMA (50 ng/ml) and/or CCL3 (103 ng/ml) for 24 h. Representative images from four independent experiments are shown. d–f Semi-quantitation was performed on the band intensities: d p-p38/p38 ratios, e p-JNK/JNK ratios, and f p-ERK/ERK ratios (n = 4 independent experiments). **P < 0.01, *P < 0.05, vs. no stimulation. g The effects of a p38 inhibitor (SB203580) or an ERK inhibitor (PD98059) on Mmp9 expression in WT macrophages stimulated by PMA and/or CCL3 for 24 h (n = 4 independent experiments). **P < 0.01, vs. no stimulation. h The effects of a p38 inhibitor on CaCl2-induced AAA formation. Aortic diameters were measured in vehicle-treated and SB239063-treated mice before and 6 week after CaCl2 application. (Pre: n = 5 each; 6 week- n = 5 each in-vehicle and). **P < 0.01, vs. pretreatment in each group; ##P < 0.01, SB239063 vs. vehicle. One-way ANOVA followed by Dunnett’s post hoc test was used in (a), (b), and (d–g). Unpaired two-sided Student’s t test was used in (h). Data are presented as mean values ± SEM.
