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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 4. CXCL10 gene expression and secretion is β-Catenin and cAMP dependent.

Figure 4

WT and FPC-defective cholangiocytes (FPC−) were transfected with specific siRNAs for β-Catenin or with scrambled siRNA. RNA, protein and supernatant were collected 48 hours post transfection. A) β-Catenin gene expression was reduced in WT and FPC-defective cholangiocytes transfected with the β-Catenin siRNA. B) β-Catenin protein expression was reduced in FPC-defective cholangiocytes transfected with the β-Catenin siRNA. C) Cxcl10 gene expression was significantly reduced only in FPC-defective cholangiocytes silenced for β-Catenin. D) In the same way, CXCL10 protein levels measured by ELISA in cell supernatants were reduced only in FPC-defective cholangiocytes (n=6). E, F) WT and FPC-defective cholangiocytes (FPC−) were treated with cAMP or PKA inhibitor for 24 hours. β-Catenin gene expression and secretion was increased upon cAMP treatment and decreased upon PKA inhibition only in FPC-defective cholangiocytes and not in WT cells (*p<0.05, ANOVA with post hoc corrections). FPC−: Fibrocystin-defective cholangiocytes.