Document Detail

Pressure activates rat pancreatic stellate cells.
MedLine Citation:
PMID:  15319186     Owner:  NLM     Status:  MEDLINE    
Pancreatic stellate cells (PSCs) play a central role in development of pancreatic fibrosis. In chronic pancreatitis, pancreatic tissue pressure is higher than that of the normal pancreas. We here evaluate the effects of pressure on the activation of rat PSCs. PSCs were isolated from the pancreas of Wistar rat using collagenase digestion and centrifugation with Nycodenz gradient. Pressure was applied to cultured rat PSCs by adding compressed helium gas into the pressure-loading apparatus to raise the internal pressure. Cell proliferation rate was assessed by 5-bromo-2'-deoxyuridine (BrdU) incorporation. MAPK protein levels and alpha-smooth muscle actin (alpha-SMA) expression were evaluated by Western blot analysis. Concentration of activated transforming growth factor-beta1 (TGF-beta1) secreted from PSCs into culture medium was determined by ELISA. Collagen type I mRNA expression and collagen secretion were assessed by quantitative PCR and Sirius red dye binding assay, respectively. Application of pressure significantly increased BrdU incorporation and alpha-SMA expression. In addition, pressure rapidly increased the phosphorylation of p44/42 and p38 MAPK. Treatment of PSCs with an MEK inhibitor and p38 MAPK inhibitor suppressed pressure-induced cell proliferation and alpha-SMA expression, respectively. Moreover, pressure significantly promoted activated TGF-beta1 secretion, collagen type I mRNA expression, and collagen secretion. Our results demonstrate that pressure itself activates rat PSCs and suggest that increased pancreatic tissue pressure may accelerate the development of pancreatic fibrosis in chronic pancreatitis.
Shiro Watanabe; Yoshikuni Nagashio; Hiroshi Asaumi; Yoko Nomiyama; Masashi Taguchi; Mitsuo Tashiro; Yasuyuki Kihara; Hayato Nakamura; Makoto Otsuki
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Publication Detail:
Type:  Journal Article     Date:  2004-08-19
Journal Detail:
Title:  American journal of physiology. Gastrointestinal and liver physiology     Volume:  287     ISSN:  0193-1857     ISO Abbreviation:  Am. J. Physiol. Gastrointest. Liver Physiol.     Publication Date:  2004 Dec 
Date Detail:
Created Date:  2004-11-09     Completed Date:  2004-12-20     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:  G1175-81     Citation Subset:  IM    
Third Department of Internal Medicine, University of Occupational and Environmental Health, Japan, School of Medicine, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan.
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MeSH Terms
Actins / metabolism
Blotting, Western
Cell Proliferation / drug effects
Cell Separation
Cells, Cultured
Collagen / biosynthesis
Enzyme Inhibitors / pharmacology
Enzyme-Linked Immunosorbent Assay
Extracellular Matrix / physiology
Imidazoles / pharmacology
Mitogen-Activated Protein Kinases / antagonists & inhibitors,  metabolism
Muscle, Smooth / metabolism
Pancreas / cytology*,  pathology,  physiology*
Physical Stimulation
Pyridines / pharmacology
RNA, Messenger / biosynthesis
Reverse Transcriptase Polymerase Chain Reaction
Transforming Growth Factor beta / metabolism
p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors
Reg. No./Substance:
0/Actins; 0/Enzyme Inhibitors; 0/Imidazoles; 0/Pyridines; 0/RNA, Messenger; 0/SB 203580; 0/Transforming Growth Factor beta; 9007-34-5/Collagen; EC Protein Kinases; EC Mitogen-Activated Protein Kinases

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

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