Fig. 6.
β-catenin-deficient acinar cells are not preferentially injured during caerulein-induced pancreatitis. Control and ABKO mice received tamoxifen at 2 months of age and were treated with caerulein 1 week later to induce acute pancreatitis. The extent of acinar cell regeneration was analyzed histologically on wax sections, and quantitatively by immunofluorescence on frozen sections. (A–D) 2 days after the injection series was complete, H&E staining revealed no abnormalities in the pancreata of saline-treated mice, and a similar appearance of overall injury between caerulein-treated control and ABKO mice. At this stage, acute pancreatitis is manifested by infiltrating fibroblasts and inflammatory cells (black arrowheads) and the presence of dilated, metaplastic acini (open arrowheads). is, islet; du, duct. (E–H) A similar extent and distribution of EYFP labeling (green) is observed among amylase+ acinar cells (red) of saline- and caerulein-treated mice, regardless of genotype. (I) Quantification reveals no significant difference in the percentage of R26REYFP-labeled acinar cells, between treatments or genotypes (n=4–5 mice per genotype per treatment group). (J–L) At 2 days after caerulein treatment, double-staining for EYFP (green) and the apoptosis marker cleaved caspase-3 (red) reveals no increase in apoptosis among R26REYFP-labeled acinar cells of control and ABKO mice (n=3 mice per genotype). White arrowheads indicate cCasp3+ cells, co-expressing EYFP (closed) or unlabeled (open). Scale bars: 100 μm.