Figure 2.

In pancreatitis, defective cathepsin processing/activation, resulting in impaired autophagy, causes accumulation of large autophagic vacuoles and active trypsin in acinar cells. (A). Electron micrograph showing abnormally large autophagic vacuoles in pancreas of a rat with cerulein pancreatitis. Boxed area demonstrates various types of autophagic vacuoles containing intact or partially degraded cargo (e.g., zymogen granules). (B). Schematic illustrating the hypothesis that in pancreatitis, the pathologic, intra-acinar trypsin accumulation results from an imbalance between the activities of CatB, which converts trypsinogen to trypsin, and CatL, which degrades both trypsin and trypsinogen. The stimulatory and inhibitory effects of pancreatitis on these cathepsins are shown by (+) and (−) symbols, respectively.