Literature DB >> 9220428

Morphology of the exocrine pancreas related to pancreatitis.

D E Bockman1.   

Abstract

It has been assumed in the past that pancreatic acinar cells represent an irreversible end stage in development. Consequently, when there was an increase in structures that had the morphology of ductules, the interpretation was that they were derived from the proliferation of stem cells and/or pre-existing ductular cells. Pancreatitis, however, is regressive in nature [Bockman (1984) In: Pancreatitis: Concepts and Classification. Gyr, K.E., Singer, M.V., Sarles, H., eds. Elsevier, Amsterdam, pp. 11-15]. That is, it is characterized by parenchymal destruction and loss, rather than by expansion of parenchyma. Furthermore, it was assumed that the organization of the pancreatic parenchyma is like bunches of grapes, with spheroidal acini representing the grapes, and the ductules representing the stems. Given this organization, it would be difficult to understand how regressive changes could lead to clusters of ductular structures. Investigations using three-dimensional reconstruction and retrograde injections have altered our idea of pancreatic organization. In addition to spheroidal acini, there also are other shapes, including tubular acini. Moreover, ductules do not necessarily stop when they encounter an acinus. They may emerge on the other side. Combined ductular and acinar lumina may anastomose with each other. It is now clear that pancreatic acini may undergo redifferentiation, taking on the morphology of ductules and forming tubular complexes during pancreatitis, as well as in response to pancreatic cancer, cystic fibrosis, or blockage of the ductal system. With this understanding of pancreatic architecture and morphological plasticity, it is easier to understand the changes one sees with pancreatic diseases.

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Year:  1997        PMID: 9220428     DOI: 10.1002/(SICI)1097-0029(19970601)37:5/6<509::AID-JEMT13>3.0.CO;2-U

Source DB:  PubMed          Journal:  Microsc Res Tech        ISSN: 1059-910X            Impact factor:   2.769


  24 in total

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2.  Persistent expression of PDX-1 in the pancreas causes acinar-to-ductal metaplasia through Stat3 activation.

Authors:  Takeshi Miyatsuka; Hideaki Kaneto; Toshihiko Shiraiwa; Taka-aki Matsuoka; Kaoru Yamamoto; Ken Kato; Yumiko Nakamura; Shizuo Akira; Kiyoshi Takeda; Yoshitaka Kajimoto; Yoshimitsu Yamasaki; Eric P Sandgren; Yoshiya Kawaguchi; Christopher V E Wright; Yoshio Fujitani
Journal:  Genes Dev       Date:  2006-06-01       Impact factor: 11.361

3.  Combined bicarbonate conductance-impairing variants in CFTR and SPINK1 variants are associated with chronic pancreatitis in patients without cystic fibrosis.

Authors:  Alexander Schneider; Jessica Larusch; Xiumei Sun; Amy Aloe; Janette Lamb; Robert Hawes; Peter Cotton; Randall E Brand; Michelle A Anderson; Mary E Money; Peter A Banks; Michele D Lewis; John Baillie; Stuart Sherman; James Disario; Frank R Burton; Timothy B Gardner; Stephen T Amann; Andres Gelrud; Ryan George; Matthew J Rockacy; Sirvart Kassabian; Jeremy Martinson; Adam Slivka; Dhiraj Yadav; Nevin Oruc; M Michael Barmada; Raymond Frizzell; David C Whitcomb
Journal:  Gastroenterology       Date:  2010-10-25       Impact factor: 22.682

4.  Caerulin-induced pancreatitis in rats: histological and genetic expression changes from acute phase to recuperation.

Authors:  Javier Magaña-Gómez; Guillermo López-Cervantes; Ana María Calderón de la Barca
Journal:  World J Gastroenterol       Date:  2006-07-07       Impact factor: 5.742

5.  Valproic Acid Limits Pancreatic Recovery after Pancreatitis by Inhibiting Histone Deacetylases and Preventing Acinar Redifferentiation Programs.

Authors:  John F Eisses; Angela Criscimanna; Zachary R Dionise; Abrahim I Orabi; Tanveer A Javed; Sheharyar Sarwar; Shunqian Jin; Lili Zhou; Sucha Singh; Minakshi Poddar; Amy W Davis; Akif Burak Tosun; John A Ozolek; Mark E Lowe; Satdarshan P Monga; Gustavo K Rohde; Farzad Esni; Sohail Z Husain
Journal:  Am J Pathol       Date:  2015-10-23       Impact factor: 4.307

6.  Acinar cell apoptosis and the origin of tubular complexes in caerulein-induced pancreatitis.

Authors:  L E Reid; N I Walker
Journal:  Int J Exp Pathol       Date:  1999-08       Impact factor: 1.925

7.  Massive acinar cell apoptosis with secondary necrosis, origin of ducts in atrophic lobules and failure to regenerate in cyanohydroxybutene pancreatopathy in rats.

Authors:  L Kelly; L Reid; N I Walker
Journal:  Int J Exp Pathol       Date:  1999-08       Impact factor: 1.925

8.  Pancreatic stellate cells contribute to regeneration early after acute necrotising pancreatitis in humans.

Authors:  A Zimmermann; B Gloor; A Kappeler; W Uhl; H Friess; M W Büchler
Journal:  Gut       Date:  2002-10       Impact factor: 23.059

9.  Severe pancreatitis with exocrine destruction and increased islet neogenesis in mice with suppressor of cytokine signaling-1 deficiency.

Authors:  Ye Chen; Mark M W Chong; Rima Darwiche; Helen E Thomas; Thomas W H Kay
Journal:  Am J Pathol       Date:  2004-09       Impact factor: 4.307

10.  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

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