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. Author manuscript; available in PMC: 2016 Jan 1.
Published in final edited form as: Cell Mol Gastroenterol Hepatol. 2015 Jan;1(1):55–74.e1. doi: 10.1016/j.jcmgh.2014.08.001

Figure 12. Anti-fibrogenic effect of cathelicidin is ERK dependent.

Figure 12

(A) Human primary normal intestinal fibroblasts were pretreated with DMSO, MEK1 inhibitor PD98059 (10 µM) or MEK1/2 inhibitor U0126 (10 µM) for 30 minutes, followed by LL-37 (5 µM) or TFA 0.1% and/or TGF-β1 (5 ng/ml) exposure for 48 hours. Pro-COL1A1 and GAPDH protein expression was detected by Western blot. Blockade of ERK partially reversed anti-fibrogenic effects of cathelicidin. (B) Human primary normal intestinal fibroblasts were exposed to LL-37 (1–10 µM) or TFA 0.1% and/or TGF-β1 (50 ng/ml) and IGF-1 (10 ng/ml) together or TGF-β1 (5 ng/ml) alone for 30 minutes. Cathelicidin activated ERK phosphorylation in human fibroblasts.