Document Detail

Transmural pressure loading enhances gastric mucosal cell proliferation.
MedLine Citation:
PMID:  22644739     Owner:  NLM     Status:  MEDLINE    
AIM: Although increased intraluminal pressure in the stomach due to gastric outlet obstruction or functional gastric motor dysfunction, including gastroparesis, may affect gastric mucosal integrity, the direct effect of mechanical pressure on gastric mucosal cells has not yet been fully investigated. The aims of this study were to determine whether exposure to transmural pressure would affect the proliferation of gastric mucosal cells and to elucidate the intracellular signaling pathways involved.
METHODS: Cellular proliferation and DNA synthesis were evaluated in rat gastric epithelial cells exposed to high transmural pressures. The levels of activation of 3 MAP kinases, ERK, JNK, and p38, were assessed, and the induction of immediate early gene expression was examined. The activation of nuclear factor activator protein-1 (AP-1) was evaluated by an electrophoretic mobility shift assay.
RESULTS: Exposure to high transmural pressure significantly increased DNA synthesis within 24 h, with the most marked increase observed after exposure to a pressure of 80 mmHg, and this increase was inhibited by the MEK1 inhibitor PD98059. Early activation of ERK kinase, but not of JNK or p38 kinase, was detected after pressure loading. Early induction of the c-fos and c-myc genes and activation of the AP-1 transcription factor were also demonstrated within 3 h of exposure to 80 mmHg of pressure.
CONCLUSION: Gastric mucosal cell proliferation induced by exposure to high transmural pressure may be related to early activation of ERK, the induction of c-fos and c-myc, and the activation of AP-1.
Hiromasa Nakamizo; Hidekazu Suzuki; Soichiro Miura; Sachiko Mogami; Hiroshi Kishikawa; Hideo Yoshida; Hirofumi Matsui; Toshifumi Hibi
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-05-30
Journal Detail:
Title:  Digestive diseases and sciences     Volume:  57     ISSN:  1573-2568     ISO Abbreviation:  Dig. Dis. Sci.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-09-26     Completed Date:  2012-12-28     Revised Date:  2013-06-03    
Medline Journal Info:
Nlm Unique ID:  7902782     Medline TA:  Dig Dis Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2545-54     Citation Subset:  AIM; IM    
Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
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MeSH Terms
Cell Line
Cell Proliferation*
DNA / biosynthesis,  metabolism
Flavonoids / pharmacology
Gastric Mucosa / cytology*
Gene Expression Regulation, Enzymologic / drug effects,  physiology
Immediate-Early Proteins / genetics,  metabolism
Mitogen-Activated Protein Kinase Kinases / genetics,  metabolism
Protein Binding
Proto-Oncogene Proteins c-fos / genetics,  metabolism
Proto-Oncogene Proteins c-myc / genetics,  metabolism
Rats, Wistar
Transcription Factor AP-1 / genetics,  metabolism
Reg. No./Substance:
0/2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0/Flavonoids; 0/Immediate-Early Proteins; 0/Proto-Oncogene Proteins c-fos; 0/Proto-Oncogene Proteins c-myc; 0/Transcription Factor AP-1; 9007-49-2/DNA; EC Protein Kinase Kinases

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

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