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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0001455,
umls-concept:C0016030,
umls-concept:C0016601,
umls-concept:C0017262,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0035696,
umls-concept:C0086418,
umls-concept:C0086661,
umls-concept:C0185117,
umls-concept:C0205263,
umls-concept:C0243126,
umls-concept:C0301630,
umls-concept:C0332283,
umls-concept:C1157645,
umls-concept:C2911684
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pubmed:issue |
1
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pubmed:dateCreated |
1989-2-23
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pubmed:abstractText |
We have studied the effect of increased intracellular levels of cyclic AMP on the growth response to platelet-derived growth factor (PDGF) of human foreskin fibroblasts in culture. It was found that forskolin, a potent stimulator of adenylate cyclase activity, inhibits the stimulatory effect of PDGF on 3H-thymidine incorporation with a dose dependence similar to that observed with regard to cyclic AMP formation. A time-course study indicated that forskolin has no effect on ongoing DNA synthesis but affects events in the prereplicative phase. The cell-cycle block induced by forskolin was found to be reversible; after removal of the drug, DNA synthesis was initiated after a lag period, similar to that of the prereplicative phase of control cells. Forskolin had no effect on PDGF binding, receptor autophosphorylation, or c-fos mRNA expression. However, a reduction in PDGF-induced c-myc mRNA expression was observed in cultures given forskolin. Forskolin was also found to have a marked stimulatory effect on the expression of interferon-beta 2 mRNA expression. However, we were unable to demonstrate that the growth-inhibitory effect of forskolin is mediated by interferon-beta. In conclusion, an increase in cAMP levels leads to a reversible inhibition of PDGF-induced DNA synthesis in human fibroblasts, which may be related to an inhibition of c-myc mRNA expression.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Forskolin,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Platelet-Derived Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Thymidine
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0021-9541
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
138
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
17-23
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:2536035-Cell Line,
pubmed-meshheading:2536035-Cyclic AMP,
pubmed-meshheading:2536035-Fibroblasts,
pubmed-meshheading:2536035-Forskolin,
pubmed-meshheading:2536035-Humans,
pubmed-meshheading:2536035-Interferon Type I,
pubmed-meshheading:2536035-Oncogenes,
pubmed-meshheading:2536035-Phosphorylation,
pubmed-meshheading:2536035-Platelet-Derived Growth Factor,
pubmed-meshheading:2536035-RNA, Messenger,
pubmed-meshheading:2536035-Thymidine
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pubmed:year |
1989
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pubmed:articleTitle |
Induction of cyclic AMP synthesis by forskolin is followed by a reduction in the expression of c-myc messenger RNA and inhibition of 3H-thymidine incorporation in human fibroblasts.
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pubmed:affiliation |
Department of Pathology, University Hospital, Uppsala, Sweden.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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