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      Clusterin is highly expressed in tubular complexes during spontaneous pancreatitis of spontaneous hypertensive rats

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          Abstract

          Pancreatitis is an inflammatory disorder of pancreas which leads to varying degrees of pancreatic endocrine and exocrine dysfunction and manifests in either acute or chronic forms. Spontaneous pancreatitis in experimental animals has rarely been reported. Here, we found acute to chronic courses of spontaneous pancreatitis in spontaneously hypertensive rats (SHRs), showing the formation of tubular complexes (TCs) and enhanced islet regeneration. We investigated the expression pattern of clusterin in the pancreas of SHRs based on immunohistochemistry (IHC). IHC analysis revealed the strong expression of clusterin in dedifferentiated duct-like cells and regenerative islets of TCs. These results imply that clusterin might be involved in the formation of TCs and parenchymal regeneration during rat pancreatitis.

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          Beta-catenin blocks Kras-dependent reprogramming of acini into pancreatic cancer precursor lesions in mice.

          David Cano, Edward Morris, Shigeki Sekine … (2010)
          Cellular plasticity in adult organs is involved in both regeneration and carcinogenesis. WT mouse acinar cells rapidly regenerate following injury that mimics acute pancreatitis, a process characterized by transient reactivation of pathways involved in embryonic pancreatic development. In contrast, such injury promotes the development of pancreatic ductal adenocarcinoma (PDA) precursor lesions in mice expressing a constitutively active form of the GTPase, Kras, in the exocrine pancreas. The molecular environment that mediates acinar regeneration versus the development of PDA precursor lesions is poorly understood. Here, we used genetically engineered mice to demonstrate that mutant Kras promotes acinar-to-ductal metaplasia (ADM) and pancreatic cancer precursor lesion formation by blocking acinar regeneration following acute pancreatitis. Our results indicate that beta-catenin is required for efficient acinar regeneration. In addition, canonical beta-catenin signaling, a pathway known to regulate embryonic acinar development, is activated following acute pancreatitis. This regeneration-associated activation of beta-catenin signaling was not observed during the initiation of Kras-induced acinar-to-ductal reprogramming. Furthermore, stabilized beta-catenin signaling antagonized the ability of Kras to reprogram acini into PDA preneoplastic precursors. Therefore, these results suggest that beta-catenin signaling is a critical determinant of acinar plasticity and that it is inhibited during Kras-induced fate decisions that specify PDA precursors, highlighting the importance of temporal regulation of embryonic signaling pathways in the development of neoplastic cell fates.
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            Models of acute and chronic pancreatitis.

            Fred Gorelick, Markus M. Lerch (2013)
            Animal models of acute and chronic pancreatitis have been created to examine mechanisms of pathogenesis, test therapeutic interventions, and study the influence of inflammation on the development of pancreatic cancer. In vitro models can be used to study early stage, short-term processes that involve acinar cell responses. Rodent models reproducibly develop mild or severe disease. One of the most commonly used pancreatitis models is created by administration of supraphysiologic concentrations of caerulein, an ortholog of cholecystokinin. Induction of chronic pancreatitis with factors thought to have a role in human disease, such as combinations of lipopolysaccharide and chronic ethanol feeding, might be relevant to human disease. Models of autoimmune chronic pancreatitis have also been developed. Most models, particularly of chronic pancreatitis, require further characterization to determine which features of human disease they include. Copyright © 2013 AGA Institute. Published by Elsevier Inc. All rights reserved.
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              Prevalence and histopathologic characteristics of pancreatitis in cats.

              H De Cock, M A Forman, T B Farver … (2007)
              Despite the high prevalence of feline pancreatic disease, no detailed description on the histopathologic nature of this disease is currently available in the literature. In this study we characterize the distribution and histopathologic changes commonly found in feline pancreases, correlate the lesions with age and gastrointestinal GI and extra-gastrointestinal disease, and compare the pancreatic lesions in cats with those in humans. The entire pancreas was removed and examined from 115 cats presented for necropsy irrespective of the cause of death. Histologic sections from left limb, right limb, and body were scored for lesions of acute (AP) and chronic pancreatitis (CP) with a scoring system based on similar systems used in human and veterinary literature. The lesions of CP in cats resemble CP in humans, with fibrosis being more prominent than inflammatory changes. Cystic degeneration gradually increased as other lesions of CP were more prominent. A distinct nodular change of zymogen depletion and acinar cell dysplasia not associated with pancreatitis was prominent in 15.6% of the pancreases. Histologically, AP consisted of neutrophilic inflammation associated with interstitial edema and necrosis of mesenteric fat. An overall prevalence of 67%, and 45% in clinically normal animals, was identified. CP was found in 69 (60.0%) pancreases, and 58 (50.4%) had CP only, with a significant correlation between age and occurrence of CP. There was a statistically significant higher prevalence of CP in the left limb in animals with gastrointestinal disease. AP was present in 18 animals (15.7%) of which 7 animals had AP only (6.1%).
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Vet Med Sci
                Journal ID (iso-abbrev): J. Vet. Med. Sci
                Journal ID (publisher-id): JVMS
                Title: The Journal of Veterinary Medical Science
                Publisher: The Japanese Society of Veterinary Science
                ISSN (Print): 0916-7250
                ISSN (Electronic): 1347-7439
                Publication date (Electronic): 16 August 2018
                Publication date (Print): October 2018
                Volume: 80
                Issue: 10
                Pages: 1553-1557
                Affiliations
                [1) ]Laboratory of Developmental Biology and Genomics, BK21 Program Plus for Advanced Veterinary Science, and Research Institute for Veterinary Science, College of Veterinary Medicine, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, 08826, Korea
                [2) ]Korea Mouse Phenotyping Center (KMPC), 1 Gwanak-ro, Gwanak-gu, Seoul, 08826, Korea
                [3) ]Severance Biomedical Science Institute, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, 50 Yonsei-ro, Seodaemun-gu, Seoul, 03722, Korea
                [4) ]College of Pharmacy, Gachon University, 1342 Seongnam-daero, Sujeong-gu, Seongnam-si Gyeonggi-do, 13120, Korea
                [5) ]Department of Veterinary Internal Medicine, College of Veterinary Medicine, Jeju National University, 61 Iljudong-ro, Jeju-si Jeju-do, 63294, Korea
                [6) ]Department of Medical Genetics and Experimental Animal Center, College of Medicine, Hallym University, 1 Hallimdaehak-gil, Chuncheon-si, Gangwon-do, 24252, Korea
                [7) ]Department of Anatomy and Cell Biology, BK21 Program Plus for Advanced Veterinary Science, and Research Institute for Veterinary Science, College of Veterinary Medicine, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, 08826, Korea
                [8) ]Interdisciplinary Program for Bioinformatics, Program for Cancer Biology and BIO-MAX/N-Bio Institute, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, 08826, Korea
                Author notes
                [* ]Correspondence to: Seong, J. K.: snumouse@ 123456snu.ac.kr
                Article
                Publisher ID: 18-0205
                DOI: 10.1292/jvms.18-0205
                PMC ID: 6207517
                PubMed ID: 30111670
                SO-VID: 5cdc36c7-af40-4f70-9d35-f4ef7450ad19
                Copyright © ©2018 The Japanese Society of Veterinary Science
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives (by-nc-nd) License. (CC-BY-NC-ND 4.0: https://creativecommons.org/licenses/by-nc-nd/4.0/ )

                History
                Date received : 12 April 2018
                Date accepted : 05 August 2018
                Categories
                Subject: Laboratory Animal Science
                Subject: Note

                Keywords: clusterin,pancreatitis,spontaneous hypertensive rat,tubular complex
                Data availability:
                Keywords: clusterin, pancreatitis, spontaneous hypertensive rat, tubular complex

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