scholarly journals Inflammatory diseases of the pancreas: what new do we know about the mechanisms of their development in the 21st century?

2021 ◽  
Vol 93 (1) ◽  
pp. 66-70
Author(s):  
Vadim A. Akhmedov ◽  
Olga V. Gaus
Keyword(s):  
Chronic Pancreatitis ◽  
Tight Junctions ◽  
21St Century ◽  
Genetic Factors ◽  
Inflammatory Diseases ◽  
Adherens Junctions ◽  
Transmembrane Proteins ◽  
Laboratory Diagnostics ◽  
Acute And Chronic Pancreatitis

Inflammatory diseases of the pancreas can range from acute to acute recurrent and chronic pancreatitis. With the improvement of laboratory diagnostics in the 21st century, the mechanisms of the pro-inflammatory and anti-inflammatory role of tight junctions, in particular the transmembrane proteins occludin, claudine and JAMs, cytoplasmic Zo-proteins, and adherens junctions, in particular -catenin, -catenin, E-cadherin, selectins and ICAMs in the pathogenesis of acute and chronic pancreatitis have become more clear. The study of genetic factors in the development of acute and chronic pancreatitis showed the role of mutations in the genes SPINK1 N34S, PRSS1, CEL-HYB in the progression of the disease.

The Role of Octreotide and Somatostatin in Acute and Chronic Pancreatitis

Digestion ◽  
1999 ◽  
Vol 60 (2) ◽  
pp. 23-31 ◽  
Author(s):  
W. Uhl ◽  
S.E. Anghelacopoulos ◽  
H. Friess ◽  
M.W. Büchler
Keyword(s):  
Chronic Pancreatitis ◽  
Acute And Chronic Pancreatitis

scholarly journals The Interaction of JRAB/MICAL-L2 with Rab8 and Rab13 Coordinates the Assembly of Tight Junctions and Adherens Junctions

2008 ◽  
Vol 19 (3) ◽  
pp. 971-983 ◽  
Author(s):  
Rie Yamamura ◽  
Noriyuki Nishimura ◽  
Hiroyoshi Nakatsuji ◽  
Seiji Arase ◽  
Takuya Sasaki
Keyword(s):  
Plasma Membrane ◽  
Epithelial Cells ◽  
Tight Junctions ◽  
Binding Protein ◽  
Adherens Junctions ◽  
Binding Domain ◽  
Endocytic Recycling ◽  
E Cadherin

The assembly of tight junctions (TJs) and adherens junctions (AJs) is regulated by the transport of integral TJ and AJ proteins to and/or from the plasma membrane (PM) and it is tightly coordinated in epithelial cells. We previously reported that Rab13 and a junctional Rab13-binding protein (JRAB)/molecule interacting with CasL-like 2 (MICAL-L2) mediated the endocytic recycling of an integral TJ protein occludin and the formation of functional TJs. Here, we investigated the role of Rab13 and JRAB/MICAL-L2 in the transport of other integral TJ and AJ proteins claudin-1 and E-cadherin to the PM by using a Ca2+-switch model. Although knockdown of Rab13 specifically suppressed claudin-1 and occludin but not E-cadherin transport, knockdown of JRAB/MICAL-L2 and expression of its Rab13-binding domain (JRAB/MICAL-L2-C) inhibited claudin-1, occludin, and E-cadherin transport. We then identified Rab8 as another JRAB/MICAL-L2-C-binding protein. Knockdown of Rab8 inhibited the Rab13-independent transport of E-cadherin to the PM. Rab8 and Rab13 competed with each other for the binding to JRAB/MICAL-L2 and functionally associated with JRAB/MICAL-L2 at the perinuclear recycling/storage compartments and PM, respectively. These results suggest that the interaction of JRAB/MICAL-L2 with Rab8 and Rab13 coordinates the assembly of AJs and TJs.

scholarly journals The Differential Role of Human Cationic Trypsinogen (PRSS1) p.R122H Mutation in Hereditary and Nonhereditary Chronic Pancreatitis: A Systematic Review and Meta-Analysis

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Cheng Hu ◽  
Li Wen ◽  
Lihui Deng ◽  
Chenlong Zhang ◽  
Aurelia Lugea ◽  
...  
Keyword(s):  
Systematic Review ◽  
Chronic Pancreatitis ◽  
Environmental Factors ◽  
Genetic Factors ◽  
Meta Analysis ◽  
Case Control Studies ◽  
Complex Disorder ◽  
Increased Risk ◽  
Cationic Trypsinogen

Background. Environmental factors and genetic mutations have been increasingly recognized as risk factors for chronic pancreatitis (CP). ThePRSS1p.R122H mutation was the first discovered to affect hereditary CP, with 80% penetrance. We performed here a systematic review and meta-analysis to evaluate the associations ofPRSS1p.R122H mutation with CP of diverse etiology.Methods. The PubMed, EMBASE, and MEDLINE database were reviewed. The pooled odds ratio (OR) with 95% confidence intervals was used to evaluate the association of p.R122H mutation with CP. Initial analysis was conducted with all etiologies of CP, followed by a subgroup analysis for hereditary and nonhereditary CP, including alcoholic or idiopathic CP.Results. A total of eight case-control studies (1733 cases and 2415 controls) were identified and included. Overall,PRSS1p.R122H mutation was significantly associated with an increased risk of CP (OR = 4.78[1.13–20.20]). Further analysis showed p.R122H mutation strongly associated with the increased risk of hereditary CP (OR = 65.52[9.09–472.48]) but not with nonhereditary CP, both alcoholic and idiopathic CP.Conclusions. Our study showing the differential role of p.R122H mutation in various etiologies of CP indicates that this complex disorder is likely influenced by multiple genetic factors as well as environmental factors.

Sa1483 A Protective Role of IL-15 in the Pathogenesis of Acute and Chronic Pancreatitis

2016 ◽  
Vol 150 (4) ◽  
pp. S327
Author(s):  
Murli Manohar ◽  
Sathisha U. Venkateshaiah ◽  
Chandrashekara Puthanapura Mahadevappa ◽  
Alok Kumar Verma ◽  
Anil Mishra
Keyword(s):  
Chronic Pancreatitis ◽  
Protective Role ◽  
Acute And Chronic Pancreatitis

scholarly journals EMC6 regulates acinar apoptosis via APAF1 in acute and chronic pancreatitis

2020 ◽  
Vol 11 (11) ◽  
Author(s):  
Jie-hui Tan ◽  
Rong-chang Cao ◽  
Lei Zhou ◽  
Zhi-tao Zhou ◽  
Huo-ji Chen ◽  
...  
Keyword(s):  
Chronic Pancreatitis ◽  
Acinar Cell ◽  
Cell Apoptosis ◽  
Inflammatory Diseases ◽  
Inflammatory Injury ◽  
Proteomic Screen ◽  
Apoptosis Pathways ◽  
Induced Apoptosis ◽  
Acute And Chronic Pancreatitis ◽  
Functional Analyses

Abstract Treatment of acute pancreatitis (AP) and chronic pancreatitis (CP) remains problematic due to a lack of knowledge about disease-specific regulatory targets and mechanisms. The purpose of this study was to screen proteins related to endoplasmic reticulum (ER) stress and apoptosis pathways that may play a role in pancreatitis. Human pancreatic tissues including AP, CP, and healthy volunteers were collected during surgery. Humanized PRSS1 (protease serine 1) transgenic (PRSS1Tg) mice were constructed and treated with caerulein to mimic the development of human AP and CP. Potential regulatory proteins in pancreatitis were identified by proteomic screen using pancreatic tissues of PRSS1Tg AP mice. Adenoviral shRNA-mediated knockdown of identified proteins, followed by functional assays was performed to validate their roles. Functional analyses included transmission electron microscopy for ultrastructural analysis; qRT-PCR, western blotting, co-immunoprecipitation, immunohistochemistry, and immunofluorescence for assessment of gene or protein expression, and TUNEL assays for assessment of acinar cell apoptosis. Humanized PRSS1Tg mice could mimic the development of human pancreatic inflammatory diseases. EMC6 and APAF1 were identified as potential regulatory molecules in AP and CP models by proteomic analysis. Both EMC6 and APAF1 regulated apoptosis and inflammatory injury in pancreatic inflammatory diseases. Moreover, APAF1 was regulated by EMC6, induced apoptosis to injure acinar cells and promoted inflammation. In the progression of pancreatitis, EMC6 was activated and then upregulated APAF1 to induce acinar cell apoptosis and inflammatory injury. These findings suggest that EMC6 may be a new therapeutic target for the treatment of pancreatic inflammatory diseases.

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