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. Author manuscript; available in PMC: 2019 Mar 1.
Published in final edited form as: Hepatology. 2018 Feb 1;67(3):1088–1108. doi: 10.1002/hep.29577

Figure 5. The cAMP-PKA-CREB signaling pathway contributes to increased autophagy in PLD cholangiocytes.

Figure 5

Figure 5

Figure 5

(A) PKA activator, 6-Phe-cAMP, increased phosphorylation of CREB in human ADPKD cholangiocytes by 5-fold. (B) Autophagic flux was increased in 6-Phe-cAMP-treated cholangiocytes in a CREB-mediated manner since the CREB inhibitor, 666-15, abolished these effects. (C) Representative images of liver sections of untreated PCK rats (n=8) and PCK rats treated with a somatostatin analog, paseriotide (n=8). A portion of enlarged hepatic cysts (*) is shown in insets. Paseriotide decreased expression of Atg5, Atg7 and LC3 compared to untreated controls by 2-3-fold. Atg proteins are stained in red; nuclei are stained with DAPI in blue. (D) Pasireotide decreased expression of Atg5 and Atg7 in cultured human ADPKD cholangiocytes by 37% and 25%, respectively. The CREB inhibitor, 666-15, inhibited expression of Atg5 and Atg7 in PLD cholangiocytes with similar magnitude.