Literature DB >> 14673200

Differentiation of acinar cells into acinoductular cells in regenerating rat pancreas.

Takamasa Tokoro1, Ekmel Tezel, Tetsuro Nagasaka, Tetsuya Kaneko, Akimasa Nakao.   

Abstract

BACKGROUND/AIMS: Several lines of experimental data suggest that acinar cells have the potential to differentiate into ductular-like cells, and these newly formed acinoductular cells may act as (facultative) stem cells. The purpose of this study was to test this hypothesis in a model of pancreatic regeneration in rats.
METHODS: In the current study, using a 90% pancreatectomy as a rat model for pancreatic regeneration, we serially examined the pancreatic tissues in a time-dependent manner by conventional histology and immunostaining. Cell proliferation was assessed by in vivo bromodeoxyuridine (BrdU) labeling.
RESULTS: By 24 h after surgery, acini showed depleted granules with more dilated lumens (acinar ectasia). By day 2, focal regions of regeneration appeared which were separated by fibrosis and composed of ductular-like cells (tubular complexes) and acinar cells with dilated lumina. Double immunofluorescent staining revealed that both amylase and CK19 were positive in the same cells localized to the focus of regeneration from the animals on day 2, the phenotype of cells from those regions apparently reverted to acinar cells, and the regions completely disappeared by day 7. By 48 h after surgery, the number of BrdU-positive cells increased 4.3-fold in ductular cells, and 2.5-fold in acinar cells compared with control tissue.
CONCLUSION: Acinar cells through acinoductular metaplasia may be a source of pancreatic regeneration. Copyright 2003 S. Karger AG, Basel and IAP

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Year:  2003        PMID: 14673200     DOI: 10.1159/000075580

Source DB:  PubMed          Journal:  Pancreatology        ISSN: 1424-3903            Impact factor:   3.996


  7 in total

Review 1.  On approaches to the functional restoration of salivary glands damaged by radiation therapy for head and neck cancer, with a review of related aspects of salivary gland morphology and development.

Authors:  R S Redman
Journal:  Biotech Histochem       Date:  2008-06       Impact factor: 1.718

2.  Progressive metaplastic and dysplastic changes in mouse pancreas induced by cyclooxygenase-2 overexpression.

Authors:  Jennifer Kl Colby; Russell D Klein; Mark J McArthur; Claudio J Conti; Kaoru Kiguchi; Toru Kawamoto; Penny K Riggs; Amy I Pavone; Janet Sawicki; Susan M Fischer
Journal:  Neoplasia       Date:  2008-08       Impact factor: 5.715

3.  Beta cell transdifferentiation does not contribute to preneoplastic/metaplastic ductal lesions of the pancreas by genetic lineage tracing in vivo.

Authors:  Oliver Strobel; Yuval Dor; Amy Stirman; Amanda Trainor; Carlos Fernández-del Castillo; Andrew L Warshaw; Sarah P Thayer
Journal:  Proc Natl Acad Sci U S A       Date:  2007-03-07       Impact factor: 11.205

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

Authors:  John P Morris; David A Cano; Shigeki Sekine; Sam C Wang; Matthias Hebrok
Journal:  J Clin Invest       Date:  2010-01-11       Impact factor: 14.808

5.  Primary culture of pancreatic (human) acinar cells.

Authors:  Lipi Singh; Dapinder K Bakshi; Rakesh Kumar Vasishta; Sunil Kumar Arora; Siddarth Majumdar; Jai Dev Wig
Journal:  Dig Dis Sci       Date:  2008-02-02       Impact factor: 3.199

6.  In vivo lineage tracing defines the role of acinar-to-ductal transdifferentiation in inflammatory ductal metaplasia.

Authors:  Oliver Strobel; Yuval Dor; Janivette Alsina; Amy Stirman; Gregory Lauwers; Amanda Trainor; Carlos Fernández-Del Castillo; Andrew L Warshaw; Sarah P Thayer
Journal:  Gastroenterology       Date:  2007-09-14       Impact factor: 22.682

7.  Acinar-to-ductal metaplasia induced by adenovirus-mediated pancreatic expression of Isl1.

Authors:  Satsuki Miyazaki; Fumi Tashiro; Junji Fujikura; Eiji Yamato; Jun-ichi Miyazaki
Journal:  PLoS One       Date:  2012-10-15       Impact factor: 3.240

  7 in total

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