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 7
Inhibition of the protective effect of PAP1 using PAP1 knockdown in vivo. (A) Three age- and sex-matched rela^flox/flox mice were injected with SDI or PAP1 siRNA (PAP1 90 and PAP1 288) twice in an 18-hour interval (circles) and then were subjected to cerulein-induced pancreatitis (arrows). (B) Pancreatic homogenates from mice as in A were obtained and immunoblotted for PAP1. Blotting for ERK1/2 protein was used as a loading control. (C) rela^flox/flox mice were pretreated with specific and nonspecific siRNA as in A and subsequently injected with 1 i.p. dose of 50 μg/kg cerulein. One hour after injection, pancreatic nuclear protein extracts (10 μg) were subjected to gel retardation assays with an NF-κB consensus probe. (D) Representative H&E staining of pancreata from mice treated as in A. Note the increase in infiltration and massive necrosis in mice with PAP1 knockdown. (E and F) Pancreatic injury was measured by determining the enzyme activity of MPO in the pancreas (E) and LDH in the serum (F). Values are mean ± SD for independent animals (n = 3). *P < 0.05.