Fig. 8. Chi3l1 induces TF expression through the MAPK signaling pathway.

(A) LSEC, MΦ and hepatocytes were isolated from naïve (Cont) and Con A-treated WT mice (n=6 per group). The TF mRNA expression levels in these cells were measured. (B) LSEC, MΦΦ and hepatocytes were isolated from naïve WT mice. The cells were treated with rChi3l1 for 5h, and TF mRNA expression levels were measured. (C) LSECs isolated from naïve WT mice were treated with indicated doses of IFN-γ, TNF-α, and rChi3l1 that match the levels of these factors detected in vivo (Fig. 2, E&F; Fig. 1C). After 5h, TF mRNA levels were measured. (D) TSEC cells (a mouse LSEC cell line) were treated with 100ng/ml of rChi3l1 for various time periods as indicated. Activation of various signaling pathways was measured by western blotting. (E) LSECs isolated from naïve WT mice were pretreated with MAPK inhibitors for 1h, followed by rChi3l1 treatment for 5h. TF mRNA expression was measured by qRT-PCR. (F) Schematic for the involvement of Chi3l1 in CILI and Con A-induced IAOC. Results shown are from three independent experiments. P values are as indicated. Two-tailed, unpaired t test was performed in B. One-way ANOVA was performed in A, C and E.