Activation of the intrinsic fibroinflammatory program in adult pancreatic acinar cells triggered by Hippo signaling disruption
Fig 1
Acinar cell-specific Lats1/2 deletions caused pancreatic inflammation and fibrosis in adult mice.
P, PL, L1/2, PL1KO, and PL2KO mice were administrated with 180 mg/kg/d of TAM for 5 consecutive days via i.p., respectively (n = 6). Pancreata were collected at Day 5 after the final injection. (A) Histological morphology of P, L1/2, PL, PL1KO, and PL2KO mice. L1/2, PL1KO, and PL2KO mice were littermate controls. (B) Western blot showing the levels of LATS1, LATS2, phospho-YAP1, YAP1, and TAZ in P and PL mice. Tubulin was used as the internal control. (C) YAP1 and TAZ IHC staining in P and PL mice. (D) Immunofluorescence of YFP (Green) and CK19 (Red) in P and PL mice. Nuclei stained with DAPI (Blue). (E) P and PL pancreata stained with anti-CD45 antibody. (F) P and PL pancreata stained with anti-αSMA antibody, and Sirius Red, respectively. αSMA, α-smooth muscle actin; CD45, ; CK19, cytokeratin 19; IHC, immunohistochemistry; i.p., intraperitoneal; L1/2, ; LATS1, large tumor suppressor 1; P, control; PL, double knockout; PL1KO, Lats1 knockout; PL2KO, Lats2 knockout; TAM, tamoxifen; TAZ, transcriptional coactivator with PDZ binding motif; YAP1, yes-associated protein 1.