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. 2017 May 12;18(5):1044. doi: 10.3390/ijms18051044

Figure 6.

Figure 6

Figure 6

The AMPK, p38 MAPK and ERK signalling pathways cooperate with adiponectin to regulate CTGF-induced KFs proliferation, migration and ECM production. KFs were preincubated with Compound C (10 μM, an AMPK inhibitor), SB203580 (10 μM, a p38 MAPK inhibitor), SP600125 (10 μM, a JNK inhibitor), PD98059 (10 μM, a MEK inhibitor) or LY294002 (10 μM, a PI3K inhibitor) or without inhibitors. After stimulation with or without adiponectin (5 μg/mL) in the presence of CTGF (6 ng/mL) for 24 h, fibroblast proliferation and migration were measured in vitro with the CCK-8 (A) and Transwell (B) assays (n = 3), respectively; (B) a: control group, b: CTGF group, c: CTGF + adiponectin group, d: CTGF + adiponectin + Compound C group, e: CTGF + adiponectin + SB203580 group, f: CTGF + adiponectin + SP600125 group, g: CTGF + adiponectin + PD98059 group, h: CTGF + adiponectin + LY294002 group. The expression levels of the collagen I, FN and α-SMA mRNAs were determined using quantitative real-time RT-PCR ((C), n = 3). The results are representative of three independent experiments. * p < 0.05, ** p < 0.01 compared with the control cells; # p < 0.05, ## p < 0.01 compared with the CTGF-treated cells; & p < 0.05 compared with the CTGF + adiponectin-treated cells. The data are expressed as means ± SE.