Abstract | BACKGROUND & AIMS: The molecular mechanisms underlying pancreatitis are largely unknown. The goal of this study was to identify an early genetic event that correlated with pancreatitis. METHODS: RESULTS: A differentially amplified band was consistently observed early after cerulein hyperstimulation. This band was identified as a portion of the mob-1 gene, an alpha-chemokine. Northern analysis indicated that mRNAs for mob-1 and another chemokine, mcp-1, were induced after cerulein hyperstimulation in vivo. mob-1 mRNA was also induced by retrograde injection of bile salts and by cerulein in acinar cells in vitro. mob-1 protein was localized to exocrine cells in pancreata of diseased animals. Pyrrolidine dithiocarbamate inhibited both chemokine gene expression and early inflammatory characteristics of pancreatitis. CONCLUSIONS:
Chemokines are induced in acinar cells by treatments that induce pancreatitis and may play an important role in the early stages of the disease.
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Authors | T Grady, P Liang, S A Ernst, C D Logsdon |
Journal | Gastroenterology
(Gastroenterology)
Vol. 113
Issue 6
Pg. 1966-75
(Dec 1997)
ISSN: 0016-5085 [Print] United States |
PMID | 9394737
(Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Chemokine CCL2
- Chemokine CXCL10
- Chemokines
- Chemokines, CXC
- Cxcl10 protein, rat
- Cytokines
- NF-kappa B
- Pyrrolidines
- RNA, Messenger
- Thiocarbamates
- pyrrolidine dithiocarbamic acid
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Topics |
- Acute Disease
- Animals
- Chemokine CCL2
(genetics, metabolism)
- Chemokine CXCL10
- Chemokines
(antagonists & inhibitors, genetics)
- Chemokines, CXC
- Cytokines
(genetics, metabolism)
- Fluorescent Antibody Technique
- Gene Expression
(physiology)
- NF-kappa B
(antagonists & inhibitors)
- Pancreas
(pathology, physiopathology)
- Pancreatitis
(genetics, pathology)
- Pyrrolidines
(pharmacology)
- RNA, Messenger
(metabolism)
- Rats
- Thiocarbamates
(pharmacology)
- Time Factors
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