EBM Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gomez, G.
Right arrow Articles by Greeley, G. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gomez, G.
Right arrow Articles by Greeley, G. H., Jr.
Experimental Biology and Medicine 226:692-700 (2001)
© 2001 Society for Experimental Biology and Medicine


ORIGINAL ARTICLE

Acute Pancreatitis Signals Activation of Apoptosis-Associated and Survival Genes inMice

Guillermo Gomez*, Heung-Man Lee*, Qin He*, Ella W. Englander*, Tatsuo Uchida{dagger} and George H. Greeley, Jr.*,1

* Department of Surgery and
{dagger} Office of Biostatistics, The University of Texas Medical Branch, Galveston,Texas 77555

In experimental models of acute pancreatitis (AP), acinar cell death occurs by both necrosis and programmed cell death or apoptosis. Apoptosis is an active form of cell death associated with a tightly regulated expression of gene products that are either pro- or antiapoptotic. The aim of this study was to characterize pancreatic mRNA levels by Northern blotting analysis of apoptosis-associated genes used during the course of cerulein-induced AP in mice. Histone H3 mRNA levels were also examined as an indicator of cell proliferation. Acinar cell apoptosis was confirmed histologically. The findings show that AP modifies pancreatic mRNA levels of both pro- and antiapoptotic genes simultaneously. Pancreatic bclXL, bax, and p53 mRNA levels increased significantly in a temporal fashion during induction of AP. Pancreatic bcl-2 mRNA levels were unchanged during AP. Pancreatic mRNA levels of insulin-like growth factor-1 (IGF-1), a mitogen and cell survival factor, and its receptor (IGF-1R) also increased in a temporal fashion during induction of AP. In summary, this study indicates that acinar cell death during cerulein-induced AP in mice can occur by the apoptotic pathway. Since factors promoting and antagonistic for cell survival are activated simultaneously, regulation of acinar cell survival appears complex and dynamic during AP.

Key Words: apoptosis • gene products • acute pancreatitis • Western blotting • Northern blotting




This article has been cited by other articles:


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
A. S. Kowalik, C. L. Johnson, S. A. Chadi, J. Y. Weston, E. N. Fazio, and C. L. Pin
Mice lacking the transcription factor Mist1 exhibit an altered stress response and increased sensitivity to caerulein-induced pancreatitis
Am J Physiol Gastrointest Liver Physiol, April 1, 2007; 292(4): G1123 - G1132.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
O. Strobel, Y. Dor, A. Stirman, A. Trainor, C. Fernandez-del Castillo, A. L. Warshaw, and S. P. Thayer
beta cell transdifferentiation does not contribute to preneoplastic/metaplastic ductal lesions of the pancreas by genetic lineage tracing in vivo
PNAS, March 13, 2007; 104(11): 4419 - 4424.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Cell Physiol.Home page
Y. Cao, S. Adhikari, A. D. Ang, P. K. Moore, and M. Bhatia
Mechanism of induction of pancreatic acinar cell apoptosis by hydrogen sulfide
Am J Physiol Cell Physiol, September 1, 2006; 291(3): C503 - C510.
[Abstract] [Full Text] [PDF]


Home page
Physiol. GenomicsHome page
X.-L. Cui, P. Soteropoulos, P. Tolias, and R. P. Ferraris
Fructose-responsive genes in the small intestine of neonatal rats
Physiol Genomics, July 8, 2004; 18(2): 206 - 217.
[Abstract] [Full Text] [PDF]


Home page
EndocrinologyHome page
G. Wang, Y. Anini, W. Wei, X. Qi, A.-M. O'Carroll, T. Mochizuki, H.-Q. Wang, M. R. Hellmich, E. W. Englander, and G. H. Greeley Jr.
Apelin, a New Enteric Peptide: Localization in the Gastrointestinal Tract, Ontogeny, and Stimulation of Gastric Cell Proliferation and of Cholecystokinin Secretion
Endocrinology, March 1, 2004; 145(3): 1342 - 1348.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2001 by the Society for Experimental Biology and Medicine.