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Mice lacking  Sirt2  spontaneously develop tumors in multiple organs, as well as when expressed in combination with oncogenic  Kras   G12D  , leading to pancreatic tumors. Here, we report that after caerulein-induced pancreatitis,  Sirt2 -deficient mice exhibited an increased inflammatory phenotype and delayed pancreatic tissue recovery. Seven days post injury, the pancreas of  Sirt2  −/−  mice display active inflammation, whereas wild-type mice had mostly recovered. In addition, the pancreas from the  Sirt2  −/−  mice exhibited extensive tissue fibrosis, which was still present at six weeks after exposure. The mice lacking  Sirt2  also demonstrated an enhanced whole body pro-inflammatory phenotype that was most obvious with increasing age. Importantly, an accumulation of a cell population with spontaneous cancerous  Kras   G12D   mutations was observed in the  Sirt2  −/−  mice that is enhanced in the recovering pancreas after exposure to caerulein. Finally, transcriptome analysis of the pancreas of the  Sirt2  −/−  mice exhibited a pro-inflammatory genomic signature. These results suggest that loss of  Sirt2 , as well as increased age, enhanced the immune response to pancreatic injury and induced an inflammatory phenotype permissive for the accumulation of cells carrying oncogenic  Kras  mutations.

Loss of Sirt2 increases and prolongs a caerulein-induced pancreatitis permissive phenotype and induces spontaneous oncogenic Kras mutations in mice