Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2004-3-11
pubmed:abstractText
We analysed the glucocorticoid receptor (GR) regulation on the expression of insulin-like growth factor 1 (IGF-1), type I IGF receptor (IGF-1.R), IGF-binding protein 3 (IGFBP-3), urokinase-type plasminogen activator (uPA) and uPA receptor (uPA.R) mRNA in human KLE endometrial-like cells. We documented that KLE cells express IGF-1, IGF-1.R, uPA and IGFBP-3 mRNA, however not uPA.R mRNA. Exogenous administration of dexamethasone inhibited the proliferation of KLE cells without inducing apoptosis. The inhibition of dexamethasone on KLE cell proliferation was neutralized by exogenous administration of IGF-1. Furthermore, dexamethasone suppressed the expression of IGF-1 mRNA and IGF-1.R mRNA as well as the IGF-1 bioavailability in KLE cell culture media, but it did not alter the expression of uPA mRNA and IGFBP-3 mRNA in KLE cells. Since the peritoneal fluid of women with endometriosis is known to contain IGF-1, which stimulates the proliferation and inhibits the apoptosis of endometrial-like cells, it is conceivable that GR-mediated down-regulation of IGF-1 bioavailability may be of clinical relevance for endometriosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0258-851X
pubmed:author
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
43-7
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:articleTitle
Glucocorticoid receptor function suppresses insulin-like growth factor 1 activity in human KLE endometrial-like cells.
pubmed:affiliation
Department of Experimental Physiology, Medical School, University of Athens, Goudi-Athens, 115 27 Greece.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't