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. 2015 Jun 12;65(8):1333–1346. doi: 10.1136/gutjnl-2014-308553

Figure 5.

Figure 5

Pancreatitis autophagy impairment and trypsinogen activation are attenuated by genetic mitochondrial permeability transition pore (MPTP) inhibition (Ppif−/−). (A) Trypsin activity (normalised) following cholecystokinin-8 (CCK-8) (10 nM) hyperstimulation inhibited in Ppif−/− vs wilt-type (Wt) cells (mean±SEM 6 cell preparations; *p<0.05 Wt CCK-8 vs Wt controls; †p<0.05 Ppif−/− CCK-8 vs Wt CCK-8). (B) Trypsinogen and amylase content similar in unstimulated and caerulein acute pancreatitis (CER-AP) Wt vs Ppif−/− pancreata (immunoblot; re-probed for ERK1/2 to confirm equal loading; each lane from an individual animal). (C) Densitometry of LC3-II with (D) representative immunoblots of LC3-II and p62 with (E) densitometry of p62 showing increased levels of these proteins in Wt CER-AP that were both significantly attenuated in Ppif−/− mice, indicating more efficient autophagic flux (immunoblots re-probed for ERK1/2 to confirm equal loading; each lane from an individual animal; 4–6 mice per group; densitometry of LC3-II or p62 as ratios of band intensities to ERK in each sample normalised to saline-treated Wt controls, means±SEM; *p<0.01 CER-AP in Wt vs Wt controls, †p<0.05 CER-AP in Ppif−/− vs CER-AP in Wt). (F) Representative images showing attenuation of CER-AP-induced increases in LC3-II puncta by genetic MPTP inhibition in green fluorescent protein (GFP)-LC3×Ppif−/− compared with GFP-LC3 transgenic mice (upper panels show LC3 puncta in saline-treated pancreas and CER-AP for both strains; lower panels show addition of nuclear stain 4',6-diamidino-2-phenylindole (DAPI)).