Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1993-11-5
pubmed:abstractText
We have previously found that transforming growth factor-beta 1 (TGF-beta 1) inhibits the mitogenic activity of platelet-derived growth factor (PDGF) in cultures of human neonatal fibroblasts in a density-dependent fashion. In the present investigation we determined the effect of TGF-beta 1 on the PDGF alpha-receptor, which binds all PDGF isoforms, as well as on the beta-receptor, which binds only PDGF-BB with high affinity. We found that the inhibitory effect of TGF-beta 1 on PDGF-AA-induced mitogenesis was density-dependent; when dense cell cultures were preincubated with TGF-beta 1, there was an complete inhibition of 3H-thymidine incorporation, whereas the effect was less in sparse cultures. A similar density-dependent effect of TGF-beta 1 was seen in PDGF-BB treated cells, although less pronounced. The binding of 125I-labeled PDGF-AA and PDGF-BB to the alpha-receptor was significantly reduced after treatment with TGF-beta 1 in dense cultures, whereas the sparse cultures were less affected. A decrease of alpha-receptor mRNA was also seen. The levels of beta-receptor protein and mRNA were unaffected. We conclude that the growth inhibitory effect of TGF-beta 1 is cell density-dependent and involves down-regulation of PDGF alpha-receptors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0021-9541
pubmed:author
pubmed:issnType
Print
pubmed:volume
157
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
97-103
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Density-dependent inhibitory effect of transforming growth factor-beta 1 on human fibroblasts involves the down-regulation of platelet-derived growth factor alpha-receptors.
pubmed:affiliation
Department of Pathology, University Hospital, Uppsala, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't