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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1991-12-18
pubmed:abstractText
In human malignant mesothelioma cell lines elevated expression of the platelet-derived growth factor (PDGF) beta-chain (c-sis) gene was previously reported, while normal mesothelial cells barely express this gene. Expression of the PDGF A-chain gene was only slightly elevated in these cell lines compared with normal mesothelial cells. For a putative autocrine function of the produced PDGF, in these cells expression of PDGF receptors is a prerequisite. In this paper we report on the expression of PDGF alpha- and beta-receptors in normal and malignant mesothelial cells. Cultured normal mesothelial cells expressed PDGF alpha-receptor mRNA and protein and had weak to undetectable levels of the PDGF beta-receptor mRNA and protein. In contrast, malignant mesothelioma cell lines were found to express PDGF beta-receptor mRNA and protein, while PDGF alpha-receptor expression was not detectable by Northern blotting and immunoprecipitation. Binding experiments with [125I]-PDGF-AA and [125I] PDGF-BB to normal and malignant mesothelial cell lines confirmed these observations. These results suggest that autocrine stimulation of growth may occur both in cultured normal mesothelial cells (PDGF-AA acting via the alpha-receptor) and in malignant mesothelioma cell lines (PDGF-BB acting via the beta-receptor).
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
N
pubmed:pagination
2005-11
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Human malignant mesothelioma cell lines express PDGF beta-receptors whereas cultured normal mesothelial cells express predominantly PDGF alpha-receptors.
pubmed:affiliation
Department of Immunology, Erasmus University, Rotterdam, The Netherlands.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't