Document Detail

Induction of early response genes in trypsin inhibitor-induced pancreatic growth.
MedLine Citation:
PMID:  17095753     Owner:  NLM     Status:  MEDLINE    
Endogenous CCK release induced by a synthetic trypsin inhibitor, camostat, stimulates pancreatic growth; however, the mechanisms mediating this growth are not well established. Early response genes often couple short-term signals with long-term responses. To study their participation in the pancreatic growth response, mice were fasted for 18 h and refed chow containing 0.1% camostat for 1-24 h. Expression of 18 early response genes were evaluated by quantitative PCR; mRNA for 17 of the 18 increased at 1, 2, 4, or 8 h. Protein expression for c-jun, c-fos, ATF-3, Egr-1, and JunB peaked at 2 h. Nuclear localization was confirmed by immunohistochemistry of c-fos, c-jun, and Egr-1. Refeeding regular chow induced only a small increase of c-jun and none in c-fos expression. JNKs and ERKs were activated 1 h after camostat feeding as was the phosphorylation of c-jun and ATF-2. AP-1 DNA binding evaluated by EMSA showed a significant increase 1-2 h after camostat feeding with participation of c-jun, c-fos, ATF-2, ATF-3, and JunB shown by supershift. The CCK antagonist IQM-95,333 blocked camostat feeding-induced c-jun and c-fos expression by 67 and 84%, respectively, and AP-1 DNA binding was also inhibited. In CCK-deficient mice, the maximal response of c-jun induction and AP-1 DNA binding were reduced by 64 and 70%, respectively. These results indicate that camostat feeding induces a spectrum of early response gene expression and AP-1 DNA binding and that these effects are mainly CCK dependent.
Lili Guo; Maria Dolors Sans; Grzegorz T Gurda; Sae-Hong Lee; Stephen A Ernst; John A Williams
Related Documents :
2158073 - Coupled and uncoupled induction of fos and jun transcription by different second messen...
12666833 - Effects of selenium and iodine on c-fos and c-jun mrna and their protein expressions in...
12482833 - Expression of g2a, a receptor for lysophosphatidylcholine, by macrophages in murine, ra...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2006-11-09
Journal Detail:
Title:  American journal of physiology. Gastrointestinal and liver physiology     Volume:  292     ISSN:  0193-1857     ISO Abbreviation:  Am. J. Physiol. Gastrointest. Liver Physiol.     Publication Date:  2007 Feb 
Date Detail:
Created Date:  2007-02-09     Completed Date:  2007-04-16     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  100901227     Medline TA:  Am J Physiol Gastrointest Liver Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  G667-77     Citation Subset:  IM    
Dept of Molecular and Integrative Physiology, Univ of Michigan Medical School, Ann Arbor, MI 48109-0622, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Activating Transcription Factor 2 / metabolism
Activating Transcription Factor 3 / genetics,  metabolism
Carbamates / pharmacology
Cholecystokinin / deficiency,  genetics
Early Growth Response Transcription Factors / genetics,  metabolism
Extracellular Signal-Regulated MAP Kinases / metabolism
Gabexate / analogs & derivatives,  pharmacology
Gene Expression / drug effects*
Immediate-Early Proteins / genetics*,  metabolism
JNK Mitogen-Activated Protein Kinases / metabolism
Mice, Inbred ICR
Mice, Knockout
Pancreas / drug effects*,  growth & development,  metabolism
Phosphorylation / drug effects
Protein Binding / drug effects
Proto-Oncogene Proteins c-fos / genetics,  metabolism
Proto-Oncogene Proteins c-jun / genetics,  metabolism
Pyrimidinones / pharmacology
Receptors, Cholecystokinin / antagonists & inhibitors
Transcription Factor AP-1 / metabolism
Trypsin Inhibitors / pharmacology*
Grant Support
Reg. No./Substance:
0/Activating Transcription Factor 2; 0/Activating Transcription Factor 3; 0/Atf2 protein, mouse; 0/Atf3 protein, mouse; 0/Carbamates; 0/Early Growth Response Transcription Factors; 0/IQM 95333; 0/Immediate-Early Proteins; 0/Proto-Oncogene Proteins c-fos; 0/Proto-Oncogene Proteins c-jun; 0/Pyrimidinones; 0/Receptors, Cholecystokinin; 0/Transcription Factor AP-1; 0/Trypsin Inhibitors; 39492-01-8/Gabexate; 59721-28-7/FOY 305; 9011-97-6/Cholecystokinin; EC Signal-Regulated MAP Kinases; EC Mitogen-Activated Protein Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Regulation of triglyceride metabolism. I. Eukaryotic neutral lipid synthesis: "Many ways to skin ACA...
Next Document:  Mechanisms of secretion-associated shrinkage and volume recovery in cultured rabbit parietal cells.