Figure 8
Regulation of claudin-8 by JNK. HT-29/B6 monolayers were treated with JNK-inhibitors SP600125 or JNKi1 before infection. (a) In controls SP600125 caused a significant drop in Rt from initial resistance within 48 h, masking a supposedly reduced decrease in Rt in Y. enterocolitica-infected monolayers (n=11). (b) Application of JNKi1 had no effect on Rt in controls and an attenuation in Y. enterocolitica-induced Rt drop became obvious (P<0.01; n=4). (c) Western blot analyses showed enhanced JNK-phosphorylation at 10 min after infection. (d) Time course of JNK-phosphorylation in HT-29/B6 after Y. enterocolitica infection. Signals from all conditions were quantified by densitometry and the ratio of P∼JNK and JNK was determined. Values from untreated controls were set as 100% and compared with signals from Y. enterocolitica stimulation. (e) Inhibition of JNK signalling restored claudin-8 protein level significantly, but had no impact on other TJ proteins probed (n=5). (f) Densitometric quantification of TJ proteins after normalization with β-actin (n=5 or 7; *P<0.05 and **P<0.01 compared with untreated control, #P<0.05 compared with inhibitor treatment).
