Skip to main content
. 2018 Mar 2;596(8):1397–1417. doi: 10.1113/JP275453

Figure 6. ERK regulates FOXC2 activation and DLL4 expression in the developing lung.

Figure 6

A, ERK phosphorylation was quantified by immunoblotting using an anti‐phospho ERK antibody in lung homogenates obtained from TLR4+/+ and TLR4−/− mice 24 h after i.p. LPS, n ≥ 4 mice in each group. B, lung DLL4 and FOXC2 mRNA were quantified by qRT‐PCR 24 h after i.p. LPS with or without i.p. ERK‐I (20 mg kg−1), P < 0.01 (*Control vs. LPS; **LPS vs. ERK‐I + LPS), n ≥ 3 mice in each group. C and D, DLL4, FOXC2, and (p)ERK were quantified by Western blotting 24 h after i.p. LPS with or without i.p. ERK‐I, with densitometry analysis shown graphically (D), P < 0.05 (*Control vs. LPS; **LPS vs. ERK‐I + LPS), n ≥ 4 mice. E and F, lung FOXC2 phosphorylation was examined by immunoprecipitation 3 h after i.p. LPS with or without ERK‐I, and quantified by densitometry (F), P < 0.001 (*Control vs. LPS: **LPS vs. ERK‐I + LPS), n ≥ 3. G, whole lung nuclear homogenates obtained at 1, 3, and 24 h after i.p. LPS were used for the ChIP assays to quantify binding of FOXC2 to the DLL4 promotor, n ≥ 3. [Color figure can be viewed at http://wileyonlinelibrary.com]