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. Author manuscript; available in PMC: 2018 Feb 20.
Published in final edited form as: Biochem J. 2017 Feb 20;474(5):647–665. doi: 10.1042/BCJ20160704

Figure 4. Potentiating interactions between post-M3R signaling pathways govern ACh-induced MMP1 gene induction.

Figure 4

HT-29 cells were pre-incubated for 45 min with PKC-α/β1, p38-α/β, EGFR, or MEK inhibitors, and then incubated for an additional 4 h with no additional test agents (C) or with ACh (100 μM). MMP1 mRNA levels were measured by qPCR. ACh-induced MMP1 expression was attenuated by inhibitors of PKC-α/β1 (5 μM Gӧ6976, 5 μM Gӧ6983), p38-α/β (10 μM SB202190, 10 μM SB203580), EGFR (5 μM PD168393, 5 μM PD153035), and MEK (10 μM PD98059, 10 μM U0126). Pre-incubating cells with a combination of p38-α/β plus EGFR inhibitors or p38-α/β plus MEK inhibitors abolished ACh-induced MMP1 gene expression, as did pre-incubation with a combination of p38-α/β, EGFR and PKC-α/β1 inhibitors. qPCR data were normalized to GAPDH and are means of four separate experiments. C, untreated control; *P < 0.05; **P < 0.01; ***P < 0.001.