Linked Life Data

7649354

Source:http://linkedlifedata.com/resource/pubmed/id/7649354

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1995-9-28
pubmed:abstractText
The mechanisms by which the sex hormones achieve their bone-sparing effects remains unresolved. Interleukin-1 beta (IL-1 beta) is an autocrine/paracrine regulator of bone that may be produced in an estrogen-sensitive manner. The regulation of IL-1 beta production by the gonadal steroids was tested in the human osteoblastic HOBIT cell model. Dose-dependent 4-8-fold increases (P < 0.05) in IL-1 beta mRNA levels followed a 6-48 h treatment with 17 beta-estradiol or testosterone. Receptor mediation of these responses was indicated by experiments using 17 alpha-estradiol or flutamide. Tumor necrosis factor-alpha (TNF) dependent increase IL-1 beta mRNA levels were additive to the effects of the steroids. Testosterone and TNF increased IL-1 beta protein release (P < 0.05) while 17 beta-estradiol had little effect on release. The bone-sparing effects of the gonadal steroids may be accomplished, in part, through their mediation of local IL-1 beta production.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0303-7207
pubmed:author
pubmed:issnType
Print
pubmed:day
28
pubmed:volume
111
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
67-74
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Sex hormones mediate interleukin-1 beta production by human osteoblastic HOBIT cells.
pubmed:affiliation
Department of Biology, West Virginia University, Morgantown 26505-6057, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't