Figure 6.

Effect of JNK inhibition on CTGF and cell death pathway mediators in NB TGF-β1-induced lung injury. NB TGF-β1 TG and WT liter-mate control mice on dox or regular water, with or without treatment with JNKi, were sacrificed at PN10, with activation of TGF-β1 at PN7. mRNA expression of CTGF, caspase 3, FAS, and FAS-L were assessed. The noted values represent assessments in a minimum of 3 animals in each group. Independent experiments were done in the presence of the JNK pathway inhibitor. The ratios of CTGF, caspase 3, FAS, and FAS-L with β-actin were quantified by densitometery (6A-D). The figures are illustrative of a minimum of 3 experiments. NB: newborn; WT: wild type; CTGF: connective tissue growth factor; TGF-β1: transforming growth factor beta1 transgenic; Reg: regular water; Dox: doxcycline water; JNKi: JNK inhibitor. #P ≤ 0.01, ##P ≤ 0.001.

Li et al. BMC Cell Biology 2011 12:54   doi:10.1186/1471-2121-12-54
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