High Mobility Group Box-1 Promotes the Proliferation and Migration of Hepatic Stellate Cells via TLR4-Dependent Signal Pathways of PI3K/Akt and JNK
Figure 2
HMGB1 induced the activation of JNK and PI3K/Akt through TLR4.
(A) Representative of significantly elevated expressions of both TLR4 and active forms of JNK, PI3K/Akt (p-JNK, p-PI3K and p-Akt) in response to HMGB1 stimulation at different concentrations. However no change of JNK, PI3K, and Akt were detected. Relative quantification of the active and total forms of JNK, PI3K, and Akt proteins are presented in the right panel. #p<0.05, compared with 0 ng/ml HMGB1; NS, not significant. (B) After pretreated with TLR4 neutralizing antibody (10 µg/mL) for 1 h, HSCs were cocultured with HMGB1 (100 ng/ml) for 24 h and then HMGB1-enhanced expression of p-JNK, p-PI3K and p-Akt were markedly decreased. Relative quantification of the active and total forms of JNK, PI3K, and Akt proteins are presented in the right panel. *p<0.05, compared with 100 ng/ml HMGB1; NS, not significant.