en
Scientific article
English

Severe acute pancreatitis and reduced acinar cell apoptosis in the exocrine pancreas of mice deficient for the Cx32 gene

Published inGastroenterology, vol. 124, no. 2, p. 481-493
Publication date2003
Abstract

The early events leading to acinar cell injury during acute pancreatitis are poorly characterized. Signaling through gap junction channels contributes to the homeostasis of the exocrine pancreas by coordinating acinar cell activity within an acinus. To explore the role of gap junctional communication in acinar cell response to injury, we analyzed the course of acute pancreatitis induced by injection of cerulein in mice deficient for Cx32, the major gap junction protein expressed in the exocrine pancreas.

Keywords
  • Acute Disease
  • Animals
  • Apoptosis
  • Caerulein
  • Connexins/deficiency/genetics/metabolism
  • Glutathione/metabolism
  • Mice
  • Mice, Inbred C3H
  • Mice, Inbred C57BL
  • Mice, Knockout/genetics
  • Pancreas/pathology/physiopathology
  • Pancreatitis/chemically induced/pathology/physiopathology
  • Proto-Oncogene Proteins/metabolism
  • Proto-Oncogene Proteins c-bcl-2/metabolism
  • Severity of Illness Index
  • Bcl-2-Associated X Protein
Citation (ISO format)
FROSSARD, Jean-Louis et al. Severe acute pancreatitis and reduced acinar cell apoptosis in the exocrine pancreas of mice deficient for the Cx32 gene. In: Gastroenterology, 2003, vol. 124, n° 2, p. 481–493. doi: 10.1053/gast.2003.50052
Main files (1)
Article (Published version)
accessLevelRestricted
Identifiers
ISSN of the journal0016-5085
615views
0downloads

Technical informations

Creation03/07/2013 8:54:00 AM
First validation03/07/2013 8:54:00 AM
Update time03/14/2023 8:06:29 PM
Status update03/14/2023 8:06:29 PM
Last indexation01/16/2024 1:24:03 AM
All rights reserved by Archive ouverte UNIGE and the University of GenevaunigeBlack