ArticleCellular and molecular life sciences : CMLS2020
Early trypsin activation develops independently of autophagy in caerulein-induced pancreatitis in mice.
Article in Cellular and molecular life sciences : CMLS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Autophagy dysfunction in pancreatic acinar cells in acute pancreatitis: from molecular mechinery and trypsinogen activation to heterogeneity and therapeutic implications.Journal of molecular histology · 2026Review
- Pathologically relevant trypsinogen activation in pancreatitis.American journal of physiology. Gastrointestinal and liver physiology · 2026Review
- Post-translational modification crosstalk in acute pancreatitis: linking acinar stress to innate immune amplification and tissue repair.Frontiers in immunology · 2026Review
- VMP1 Constitutive Expression in Mice Dampens Pancreatic and Systemic Histopathological Damage in an Experimental Model of Severe Acute Pancreatitis.International journal of molecular sciences · 2025Article
- Deletion of the WD40 domain of ATG16L1 exacerbates acute pancreatitis, abolishes LAP-like non-canonical autophagy and slows trypsin degradation.Autophagy · 2025Article
- Trypsin in pancreatitis: The culprit, a mediator, or epiphenomenon?World journal of gastroenterology · 2024Review
- Article
- Initiation of acute pancreatitis in mice is independent of fusion between lysosomes and zymogen granules.Cellular and molecular life sciences : CMLS · 2024Article
- The integration of single-cell and bulk RNA-seq atlas reveals ERS-mediated acinar cell damage in acute pancreatitis.Journal of translational medicine · 2024Article
- Review
- Comprehensive review on the pathogenesis of hypertriglyceridaemia-associated acute pancreatitis.Annals of medicine · 2023Review
- Gelsolin inhibits autophagy by regulating actin depolymerization in pancreatic ductal epithelial cells in acute pancreatitis.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2023Article
- A Label-Free Fluorescence Aptasensor Based on G-Quadruplex/Thioflavin T Complex for the Detection of Trypsin.Molecules (Basel, Switzerland) · 2022Article
- Autophagy, Acute Pancreatitis and the Metamorphoses of a Trypsinogen-Activating Organelle.Cells · 2022Review
- Ginsenoside Rg3 ameliorates acute pancreatitis by activating the NRF2/HO‑1‑mediated ferroptosis pathway.International journal of molecular medicine · 2022Article
- The lncRNA TCONS_00021785/miR-21-5p/Trim33 axis regulates VMP1-mediated zymophagy, reduces the activation of trypsinogen, and promotes acinar cell recovery.Cell death discovery · 2022Article
- Drug discovery and formulation development for acute pancreatitis.Drug delivery · 2020Review
- Biochemical Evaluation of the Antioxidant Effects of Hydroxytyrosol on Pancreatitis-Associated Gut Injury.Antioxidants (Basel, Switzerland) · 2020Article
- Article
- Systemic Administration of Fibroblast Growth Factor 21 Improves the Recovery of Spinal Cord Injury (SCI) in Rats and Attenuates SCI-Induced Autophagy.Frontiers in pharmacology · 2020Article
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Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
Abstract
Premature intrapancreatic trypsinogen activation is widely regarded as an initiating event for acute pancreatitis. Previous studies have alternatively implicated secretory vesicles, endosomes, lysosomes, or autophagosomes/autophagolysosomes as the primary site of trypsinogen activation, from which a cell-damaging proteolytic cascade originates. To identify the subcellular compartment of initial trypsinogen activation we performed a time-resolution analysis of the first 12 h of caerulein-induced pancreatitis in transgenic light chain 3 (LC3)-GFP autophagy reporter mice. Intrapancreatic trypsin activity increased within 60 min and serum amylase within 2 h, but fluorescent autophagosome formation only by 4 h of pancreatitis in parallel with a shift from cytosolic LC3-I to membranous LC3-II on Western blots. At 60 min, activated trypsin in heavier subcellular fractions was co-distributed with cathepsin B, but not with the autophagy markers LC3 or autophagy protein 16 (ATG16). Supramaximal caerulein stimulation of primary pancreatic acini derived from LC3-GFP mice revealed that trypsinogen activation is independent of autophagolysosome formation already during the first 15 min of exposure to caerulein. Co-localization studies (with GFP-LC3 autophagosomes versus Ile-Pro-Arg-AMC trypsin activity and immunogold-labelling of lysosomal-associated membrane protein 2 [LAMP-2] versus trypsinogen activation peptide [TAP]) indicated active trypsin in autophagolysosomes only at the later timepoints. In conclusion, during the initiating phase of caerulein-induced pancreatitis, premature protease activation develops independently of autophagolysosome formation and in vesicles arising from the secretory pathway. However, autophagy is likely to regulate overall intracellular trypsin activity during the later stages of this disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.