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. 2019 Aug 14;9(1):1–13. doi: 10.1016/j.jcmgh.2019.08.003

Figure 5.

Figure 5

ASNase-induced ASNS up-regulation is mediated through PERK, and compared with the other pancreatitis triggers, only ASNase exposure leads to activation of eIF2α and up-regulation of ASNS. (A) In 266-6 acinar cells, the PERK inhibitor GSK2606414 (PERKi; 10 μmol/L) suppressed ASNase-induced up-regulation of ASNS (n = 5; *P < .05). (B) By qPCR, there was no difference in X-box binding protein 1 cleavage with ASNase (n = 3). Tunicamycin (Tun; 5 μg/mL for 6 h) served as a positive control for inducing ER stress. (C) Mouse 266-6 acinar cells were treated for 6 hours with pathologically relevant concentrations of pancreatitis stimuli. Cerulein (100 nmol/L), radiocontrast (RC; 16%), and taurolithocholic acid 3-sulfate (TLCS; 500 umol/L). (D) Pancreatic ASNS and p-PERK/total PERK in mice fasted for 12 hours (n = 4). p-PERK, phosphorylated PERK.