Pancreas-specific RelA/p65 truncation increases susceptibility of acini to inflammation-associated cell death following cerulein pancreatitis
J. Clin. Invest. Hana Algül, et al. 117:1490 doi:10.1172/JCI29882 [Go to this article.]

Figure 8
Protective effect of PAP1 on cerulein-induced pancreatitis in rela^Δ/Δ mice. (A) Lentivirus harboring the full-length cDNA of murine PAP1 was generated in HEK 293T cells and injected i.p. into rela^Δ/Δ mice to express PAP1 (pLenti4-PAP1) in the pancreas (circles). Four age- and sex-matched mice were used. Littermate control mice were infected with lentivirus (pLenti4-LacZ) containing the lacZ gene. Mice were subjected to cerulein-induced pancreatitis (arrows) 7 days after infection and then were sacrificed 12 and 24 hours after the first cerulein injection. (B) Pancreatic homogenates were obtained 12 hours after the first cerulein injection and analyzed for PAP1 expression. (C) Representative H&E-stained sections of pancreata and lungs from mice treated as in A. Original magnification, ×100. (D) To assess the extent of tissue injury, necrosis and apoptosis were evaluated. Areas of necrotic parenchymal surface were measured and quantified. TUNEL assay was used to determine the apoptotic index of the pancreas. Values are mean ± SD for independent animals (n = 4). *P < 0.05.