Fig. 4: EMC6 and APAF1 induce apoptosis and promote AP progression.
From: EMC6 regulates acinar apoptosis via APAF1 in acute and chronic pancreatitis
Histologic alteration, MPO expression, cell apoptosis, and microstructure changes in pancreatic tissues from PRSS1Tg AP mice with EMC6 inhibition by shEMC6 (A) or APAF1 inhibition by shAPAF1 (B) were measured by H&E staining, IHC, transferase-mediated d-UTP nick-end-labeling (TUNEL) assays, and TEM, respectively; black arrows (↑): cell nucleus; white arrows (↑): endoplasmic reticulum; blue arrows (↑): zymogen granule; purple arrows (↑): mitochondria; red arrows (↑): apoptotic body. Histological scores (C), MPO immunohistochemistry scores (D), and TUNEL assays (E) of pancreatic tissues in PRSS1Tg AP model after finishing EMC6 or APAF1 inhibition. F Expressions of IL-1β, IL-6, and TNF-α in pancreatic tissues from caerulein-treated PRSS1Tg mice treated with shEMC6 or shAPAF1. G Western blotting analyses of EMC6 and APAF1 expressions in pancreatic tissues from PRSS1Tg AP model; β-actin served as the internal loading control. H qRT-PCR for analysis of EMC6 and APAF1 expressions in pancreatic tissues from PRSS1Tg AP model. NC, negative control. Data represents the mean ± SD; ns, no significant difference; *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001. Scale bars (H&E, MPO) = 100 μm; scale bars (TUNEL) = 200 μm.
