Hongwei Zhu1, Xiao Yu1, Shaihong Zhu1, Xia Li2, Ben Lu3, Zhiqiang Li1, Can Yu1. 1. Department of Gastrointestinal and Pancreatic Surgery, Third Xiangya Hospital, Central South University Changsha 410013, Hunan, China. 2. Department of Endocrinology, Third Xiangya Hospital, Central South University Changsha 410013, Hunan, China. 3. Department of Hematology, Third Xiangya Hospital, Central South University Changsha 410013, Hunan, China.
Abstract
BACKGROUND & AIMS: Acute pancreatitis is an inflammatory pancreatic disease that carries considerable morbidity and mortality. The pathogenesis of this disease remains poorly understood. We investigated the incidence of autophagy in mice following induction of acute pancreatitis. METHODS: Mice were received intraperitoneal injections of L-arginine (200 mg × 2/100 g BW), while controls were administered with saline. Pancreatic tissues were assessed by histology, electron microscopy and western blotting. RESULTS: Injection of L-arginine resulted in the accumulation of autophagosomes and a relative paucity of autolysosomes. Moreover, the autophagy marker p62 is significantly increased. However, the lysosomal-associated membrane protein-2 (Lamp-2), a protein that is required for the proper fusion of autophagosomes with lysosomes, is decreased in acute pancreatitis. These results suggest that a crucial role for autophagy and Lamp-2 in the pathogenesis of acute pancreatitis. CONCLUSIONS: Our data suggest that the autophagic flux is impaired in acute pancreatitis. The depletion of Lamp-2 may play a role in the pathogenesis of acute pancreatitis.
BACKGROUND & AIMS:Acute pancreatitis is an inflammatory pancreatic disease that carries considerable morbidity and mortality. The pathogenesis of this disease remains poorly understood. We investigated the incidence of autophagy in mice following induction of acute pancreatitis. METHODS:Mice were received intraperitoneal injections of L-arginine (200 mg × 2/100 g BW), while controls were administered with saline. Pancreatic tissues were assessed by histology, electron microscopy and western blotting. RESULTS: Injection of L-arginine resulted in the accumulation of autophagosomes and a relative paucity of autolysosomes. Moreover, the autophagy marker p62 is significantly increased. However, the lysosomal-associated membrane protein-2 (Lamp-2), a protein that is required for the proper fusion of autophagosomes with lysosomes, is decreased in acute pancreatitis. These results suggest that a crucial role for autophagy and Lamp-2 in the pathogenesis of acute pancreatitis. CONCLUSIONS: Our data suggest that the autophagic flux is impaired in acute pancreatitis. The depletion of Lamp-2 may play a role in the pathogenesis of acute pancreatitis.
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