Skip to main content
. Author manuscript; available in PMC: 2016 Aug 1.
Published in final edited form as: Toxicol In Vitro. 2015 May 9;29(5):1146–1155. doi: 10.1016/j.tiv.2015.05.001

Fig. 7. Activation of the JNK signaling pathway contributes to lead-induced cytotoxicity.

Fig. 7

A-D, SGZ-aNPCs were treated with 2 μM lead for the indicated amount of time. The cell lysates were subjected to Western blot analysis for (A) phosphorylated-JNK and (C) phosphorylated c-Jun, and the fold induction of (B) p-JNK (normalized to total JNK) and (D) p-c-Jun (normalized to GAPDH) in lead-treated cells compared to DMSO controls was quantified. E-F, SGZ-aNPCs were pretreated with 0.5 μM of the ATP-competitive, pan-JNK inhibitor SP600125 for 1 h and then treated with 0.5 μM lead for an additional 48 h. Quantification of (E) the total cell number and (F) the percent apoptot ic cells. A-D: n = 2 independent experiments with duplicates . E-F: n = 3 independent experiments for a total of 9 coverslips per data point. Data represent mean ± SEM., n.s. not significant,* p < 0.05; ** p < 0.01; *** p < 0.001.