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. Author manuscript; available in PMC: 2019 May 1.
Published in final edited form as: Hepatology. 2018 Mar 25;67(5):1903–1919. doi: 10.1002/hep.29652

Figure 7. Increased IL-1β production from FPC-defective cholangiocytes is responsible for increased CXCL10 through JAK/STAT3 pathway.

Figure 7

A) Pro-IL-1β gene expression was increased in FPC-defective cholangiocytes (FPC−) compared to WT cells (n=8). B) IL-1β protein levels measured by ELISA in cell supernatant was increased in FPC-defective cholangiocytes compared to WT cell in vitro (n=8). C, D) Treatment with STAT3 inhibitor inhibited the IL-1β-induced Cxcl10 gene expression and CXCL10 protein levels in FPC-defective but not in WT cholangiocytes (n=8). E) FACS plot showed increased expression of pSTAT3(Tyr705) in FPC- defective cholangiocytes treated with IL-1β for 1 hour as compared to untreated cells and the respective quantification(n=3). F) Western blot of pSTAT3 and the respective quantification showing that the induction of pSTAT3 upon IL-1β treatment was abolished in the presence of JAK/Tyk2 inhibitor (n=3). The results in graph C and D are presented as fold change to untreated cells and the statistics were performed with the one sample Ttest (*p<0.05; Students Ttest). FPC−: Fibrocystin-defective cholangiocytes.