Linked Life Data

11700023

Source:http://linkedlifedata.com/resource/pubmed/id/11700023

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2001-11-8
pubmed:abstractText
Regulated upon activation, normal T-cells expressed and secreted (RANTES) mainly migrates memory type CD4+ T-lymphocytes to inflamed tissues. In this study, we examined effects of bile acids on RANTES gene expression in human hepatoma cells. Upon stimulation with hydrophobic bile acids, RANTES proteins were clearly increased. Semiquantitative RT-PCR analysis revealed that chenodeoxycholic acid (CDCA) induced RANTES mRNA expression. Moreover, RANTES was transcriptionally induced in two hepatoma cell lines by CDCA, presumably via its cognate NF-kappaB binding sites in the RANTES promoter. Electrophoretic mobility shift assay revealed that hydrophobic bile acids induced DNA-binding activity of NF-kappaB. Additionally, the magnitude of inducibility was closely associated with the hydrophobicity of bile acids. In conclusion, we might indicate that bile acids induced RANTES gene expression in human hepatoma cells, possibly suggesting that bile acids play an important role in migration of inflammatory cells by RANTES to the liver in patients with primary biliary cirrhosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0006-291X
pubmed:author
pubmed:copyrightInfo
Copyright 2001 Academic Press.
pubmed:issnType
Print
pubmed:day
16
pubmed:volume
288
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1095-101
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Bile acids regulate RANTES gene expression through its cognate NF-kappaB binding sites.
pubmed:affiliation
Second Department of Internal Medicine, Asahikawa Medical College, Midorigaoka higashi 2-1, Asahikawa 078-8510, Japan. fhirano@asahikawa-med.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't