Linked Life Data

3106020

Source:http://linkedlifedata.com/resource/pubmed/id/3106020

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1987-6-25
pubmed:abstractText
Control of trabecular bone volume is mediated by local events. Recently, it has been shown that the cytokines interleukin-1 (IL-1), tumor necrosis factor alpha (TNF alpha), and TNF beta [also called lymphotoxin (LT)] produced by immune cells all stimulate osteoclast activity, whereas the lymphokine interferon-gamma (IFN gamma) inhibits osteoclast activity stimulated by these agents. We report here the effects of each of these cytokines on bone collagen content measured as incorporation of proline into collagen and noncollagen protein in 20-day-old fetal rat calvariae. We found that IL-1, LT, and TNF decreased bone collagen synthesis and, to a lesser degree, noncollagen protein synthesis when the bones were exposed continuously to these agents. In addition, these cytokines stimulated DNA synthesis in the calvariae. In contrast to its action on bone resorption, where it opposed the resorptive effects of IL-1, TNF, and LT, IFN gamma inhibited bone collagen synthesis and had an additive effect with TNF and LT when bones were exposed to both. However, unlike the other cytokines, IFN gamma also decreased DNA synthesis in the calvariae. These data indicate that cytokines released by immune cells in the bone marrow microenvironment may work in concert to affect osteoblast activity in vitro.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
120
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2494-9
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Effects of interferon-gamma and other cytokines on collagen synthesis in fetal rat bone cultures.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.