Somatostatin expression in the pancreatic cells of smoking and non-smoking chronic pancreatitis patients with or without diabetes

AbstractThe molecular principles that lead to chronic pancreatitis are incompletely understood. Trypsin(ogen) plays a key role in the development of pancreatitis. Since the production of trypsin(ogen) by acinary pancreatic cells is paralleled by the expression of vigilin we hypothesised that vigilin may be involved in the onset of pancreatitis. Vigilin is a ubiquitous protein and has apparently high affinity to RNA.In the present study experimental pancreatitis was induced in male rats by a single intravenous application of dibutyltin dichloride (DBTC). Sections of rat pancreas were immunostained with an affinity-purified polyclonal antiserum against vigilin or trypsin(ogen). The changes in vigilin and trypsin(ogen) protein expression were determined by immunoblotting and subsequent sequence analysis of the amino acids.Induction of pancreatitis by DBTC caused alterations in the distribution and the amount of both vigilin and trypsin(ogen) as shown by immunohistochemical and immunoblot analysis.Furthermore we could demonstrate that anionic trypsinogen expression is up-regulated in DBTC-induced chronic pancreatitis. The obtained results suggest that vigilin as well as trypsin(ogen) are involved in the pathogenesis of pancreatitis and that the long-time DBTC-induced pancreatitis is a useful model for study of chronic pancreatitis.

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Chronic Pancreatitis and the Development of Pancreatic Cancer

Endocrine Metabolic & Immune Disorders - Drug Targets ◽

10.2174/1871530320666200423095700 ◽

2020 ◽

Vol 20 (8) ◽

pp. 1182-1210

Author(s):

Hemanth K. Kandikattu ◽

Sathisha U. Venkateshaiah ◽

Anil Mishra

Keyword(s):

Pancreatic Cancer ◽

Chronic Pancreatitis ◽

Digestive Enzymes ◽

Inflammatory Cell ◽

Stellate Cells ◽

Pancreatic Stellate Cells ◽

Inflammatory Disorder ◽

Ductal Cells ◽

Pancreatic Cells

Pancreatitis is a fibro-inflammatory disorder of the pancreas that can occur acutely or chronically as a result of the activation of digestive enzymes that damage pancreatic cells, which promotes inflammation. Chronic pancreatitis with persistent fibro-inflammation of the pancreas progresses to pancreatic cancer, which is the fourth leading cause of cancer deaths across the globe. Pancreatic cancer involves cross-talk of inflammatory, proliferative, migratory, and fibrotic mechanisms. In this review, we discuss the role of cytokines in the inflammatory cell storm in pancreatitis and pancreatic cancer and their role in the activation of SDF1α/CXCR4, SOCS3, inflammasome, and NF-κB signaling. The aberrant immune reactions contribute to pathological damage of acinar and ductal cells, and the activation of pancreatic stellate cells to a myofibroblast-like phenotype. We summarize several aspects involved in the promotion of pancreatic cancer by inflammation and include a number of regulatory molecules that inhibit that process.

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Structural modifications of intercellular junctions.

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100082510 ◽

1978 ◽

Vol 36 (2) ◽

pp. 330-331

Author(s):

J. Metz ◽

M. Merlo ◽

W. G. Forssmann

Keyword(s):

Gap Junctions ◽

Intercellular Junctions ◽

Cell Isolation ◽

Extrahepatic Cholestasis ◽

Structural Modifications ◽

Pancreatic Duct Ligation ◽

Pancreatic Cells ◽

Duct Ligation ◽

Thin Sectioning ◽

And Function

Structure and function of intercellular junctions were studied under the electronmicroscope using conventional thin sectioning and freeze-etch replicas. Alterations of tight and gap junctions were analyzed 1. of exocrine pancreatic cells under cell isolation conditions and pancreatic duct ligation and 2. of hepatocytes during extrahepatic cholestasis.During the different steps of cell isolation of exocrine pancreatic cells, gradual changes of tight and gap junctions were observed. Tight junctions, which formed belt-like structures around the apex of control acinar cells in situ, subsequently diminished, became interrupted and were concentrated into macular areas (Fig. 1). Aggregations of membrane associated particles, which looked similar to gap junctions, were intermixed within tight junctional areas (Fig. 1). These structures continously disappeared in the last stages of the isolation procedure. The intercellular junctions were finally separated without destroying the integrity of the cell membrane, which was confirmed with porcion yellow, lanthanum chloride and horse radish peroxidase.

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