Linked Life Data

8568266

Source:http://linkedlifedata.com/resource/pubmed/id/8568266

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1996-3-6
pubmed:abstractText
The therapeutic effectiveness of ursodeoxycholic acid (UDCA) for various autoimmune liver diseases strongly indicates that UDCA possesses immunomodulatory activities. Experimental evidence also supports this notion, since, for example, UDCA has been shown to suppress secretion of IL-2, IL-4, and IFN-gamma from activated T lymphocytes, and Ig production from B lymphocytes. To investigate the mechanical background of UDCA-mediated immunomodulation, we asked whether UDCA interacts with the intracellular signal transduction pathway, especially whether it is involved in immunosuppressive glucocorticoid hormone action. For this purpose, we used a cloned Chinese hamster ovary cell line, CHOpMTGR, in which glucocorticoid receptor cDNA was stably integrated. In immunocytochemical analysis, we found that treatment with UDCA promoted the nuclear translocation of the glucocorticoid receptor in a ligand-independent fashion, which was further confirmed by immunoprecipitation assays. Moreover, the translocated glucocorticoid receptor demonstrated sequence-specific DNA binding activity. Transient transfection experiments revealed that treatment of the cells with UDCA marginally enhanced glucocorticoid-responsive gene expression. We also showed that UDCA suppressed IFN-gamma-mediated induction of MHC class II gene expression via the glucocorticoid receptor-mediated pathway. Together, UDCA-dependent promotion of translocation of the glucocorticoid receptor may be associated with, at least in part, its immunomodulatory action through glucocorticoid receptor-mediated gene regulation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
156
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1601-8
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:8568266-Adjuvants, Immunologic, pubmed-meshheading:8568266-Animals, pubmed-meshheading:8568266-Base Sequence, pubmed-meshheading:8568266-CHO Cells, pubmed-meshheading:8568266-Cell Compartmentation, pubmed-meshheading:8568266-Cricetinae, pubmed-meshheading:8568266-DNA-Binding Proteins, pubmed-meshheading:8568266-Dexamethasone, pubmed-meshheading:8568266-Down-Regulation, pubmed-meshheading:8568266-Fluorescent Antibody Technique, Indirect, pubmed-meshheading:8568266-Gene Expression Regulation, pubmed-meshheading:8568266-Genes, MHC Class II, pubmed-meshheading:8568266-Glucocorticoids, pubmed-meshheading:8568266-Interferon-gamma, pubmed-meshheading:8568266-Ligands, pubmed-meshheading:8568266-Molecular Sequence Data, pubmed-meshheading:8568266-RNA, Messenger, pubmed-meshheading:8568266-Receptors, Glucocorticoid, pubmed-meshheading:8568266-Recombinant Proteins, pubmed-meshheading:8568266-Signal Transduction, pubmed-meshheading:8568266-Transcription, Genetic, pubmed-meshheading:8568266-Ursodeoxycholic Acid
pubmed:year
1996
pubmed:articleTitle
Ligand-independent activation of the glucocorticoid receptor by ursodeoxycholic acid. Repression of IFN-gamma-induced MHC class II gene expression via a glucocorticoid receptor-dependent pathway.
pubmed:affiliation
Second Department of Internal Medicine, Asahikawa Medical College, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't