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Involvement of a Stat3 binding site in inflammation-induced enteric apelin expression.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Han, Song Wang, Guiyun Qi, Xiang Englander, Ella W. Greeley, George H.
Description	Country affiliation: United States Author Affiliation: Han S ( Dept. of Surgery, Univ. of Texas Medical Branch, Galveston, TX 77555, USA.)
Abstract	Apelin is the endogenous ligand for the APJ receptor; both are expressed in the gastrointestinal tract. Experimental colitis in rodents and inflammatory bowel disease in humans are associated with increased intestinal apelin production. Our aim was to use LPS and proinflammatory cytokine-treated (IL-6 and IFN-gamma) rodents or enteric cells to identify signaling mechanisms underlying inflammation-induced enteric apelin expression. LPS, IL-6, or IFN-gamma treatment of rodents increased enteric apelin expression. Pharmacological blockade of Jak/Stat signaling or IL-6 antibody administration inhibited elevations in enteric apelin expression. Transient transfection experiments showed that LPS, IL-6, or IFN-gamma increased apelin expression by stimulation of apelin promoter activity, and blockade of Jak/Stat signaling abolished elevations in apelin promoter activity. A chromatin immunoprecipitation assay showed that IL-6 induced binding of phospho-Stat3 to a putative Stat3 site in the apelin promoter; mutation of this site abrogated the LPS-induced elevation in apelin promoter activity. Together, our findings indicate that binding of phospho-Stat3 to the apelin promoter is the final step underlying proinflammatory cytokine-induced enteric apelin expression during intestinal inflammation.
File Format	HTM / HTML
ISSN	01931857
e-ISSN	15221547
DOI	10.1152/ajpgi.90493.2008
Journal	AJP: Gastrointestinal and Liver Physiology
Issue Number	5
Volume Number	295
Language	English
Publisher	American Physiological Society
Publisher Date	2008-11-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Physiology Discipline Gastroenterology Carrier Proteins Metabolism Ileum Inflammation Stat3 Transcription Factor Adipokines Animals Genetics Cells, Cultured Gene Expression Regulation Chemically Induced Intercellular Signaling Peptides And Proteins Interferon-gamma Interleukin-6 Janus Kinases Lipopolysaccharides Mice Mice, Inbred C57bl Mice, Nude Protein Binding Rats, Sprague-dawley Stomach Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Hepatology Physiology Physiology (medical) Gastroenterology

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Involvement of a Stat3 binding site in inflammation-induced enteric apelin expression.

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Involvement of a Stat3 binding site in inflammation-induced enteric apelin expression

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Involvement of a Stat3 binding site in inflammation-induced enteric apelin expression.