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. 2012 Dec 19;7(12):e52133. doi: 10.1371/journal.pone.0052133

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© 2012 Avila et al

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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(A) Schematic of experimental design. Mice were treated with tamoxifen at 8 weeks of age to activate K-ras^G12D and delete Notch1 expression. Two weeks later, mice were treated with caerulein for 2 consecutive days to induce acute pancreatitis. Pancreatic tissue was collected 3 weeks following the final caerulein treatment. (B) Histological analysis of pancreas tissue from Elastase1-Cre^ERT2;Notch1^lox/lox, Elastase1-Cre^ERT2;Kras^G12D, and Elastase1-Cre^ERT2;Kras^G12D;Notch1^lox/lox mice following acute pancreatitis. PanIN-3 lesions are shown in Elastase1-Cre^ERT2;Kras^G12D and Elastase1-Cre^ERT2;Kras^G12D;Notch1^lox/lox pancreas tissue. Scale bar, 30 µm. (C) Fibroplasia and inflammation observed in Elastase1-Cre^ERT2;Kras^G12D and Elastase1-Cre^ERT2;Kras^G12D;Notch1^lox/lox pancreas tissue. Scale bar, 100 µm. (D) Atypical flat lesions (AFLs) were observed in Elastase1-Cre^ERT2;Kras^G12D and Elastase1-Cre^ERT2;Kras^G12D;Notch1^lox/lox pancreas tissue. Scale bar, 100 µm. (E) Analysis of the number of PanIN lesions found per pancreas in Elastase1-Cre^ERT2;Kras^G12D (n = 5) and Elastase1-Cre^ERT2;Kras^G12D;Notch1^lox/lox (n = 6) following acute pancreatitis.