Source:http://linkedlifedata.com/resource/pubmed/id/10199559
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1999-4-27
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pubmed:abstractText |
Insulin-like growth factor-I (IGF-I) is essential for normal epidermal homeostasis; however, the role of IGF binding proteins (IGFBPs), regulators of IGF action, remains unclear. Here we examine the regulation of human keratinocyte-produced IGFBPs by epidermal growth factor (EGF), transforming growth factor beta 1 (TGFbeta1), and IGF-I, growth factors known to be active in skin. In the absence of added growth factors, IGFBP-3 was the major binding protein secreted into the medium by primary keratinocytes. Addition of EGF or TGFbeta1 to keratinocyte cultures resulted in a significant decrease in IGFBP-3 abundance in conditioned medium when compared with control, untreated cells. Specifically, EGF (50 ng/ml) and TGFbeta1 (50 ng/ml) reduced IGFBP-3 abundance to 15+/-6% and 22+/-9%, respectively. Using Northern blot analysis, we found EGF and TGFbeta1 (50 ng/ml) to reduce IGFBP-3 mRNA levels in keratinocytes to 51+/-12% and 50+/-38%, respectively, when compared with control, untreated cells. Treatment with IGF-I or its analogue des(1-3)IGF-I did not lead to any consistent change in IGFBP-3 abundance. However, both IGF-I and des(1-3)IGF-I at 100 ng/ml led to a modest increase in IGFBP-3 mRNA levels in keratinocytes, suggesting posttranscriptional regulation of IGFBP-3 abundance. We propose that local modulation of IGFBP-3 abundance may represent another level of regulation of growth factor action in the epidermis, where EGF and TGFbeta1 and possibly other local growth factors specifically regulate the availability of IGF-I to its keratinocyte receptors.
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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/Culture Media, Conditioned,
http://linkedlifedata.com/resource/pubmed/chemical/Epidermal Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor Binding...,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor I,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta,
http://linkedlifedata.com/resource/pubmed/chemical/insulin-like growth factor 1...
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0021-9541
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
179
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
201-7
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:10199559-Culture Media, Conditioned,
pubmed-meshheading:10199559-Epidermal Growth Factor,
pubmed-meshheading:10199559-Gene Expression Regulation,
pubmed-meshheading:10199559-Humans,
pubmed-meshheading:10199559-Insulin-Like Growth Factor Binding Protein 3,
pubmed-meshheading:10199559-Insulin-Like Growth Factor I,
pubmed-meshheading:10199559-Keratinocytes,
pubmed-meshheading:10199559-Peptide Fragments,
pubmed-meshheading:10199559-RNA, Messenger,
pubmed-meshheading:10199559-Skin,
pubmed-meshheading:10199559-Transforming Growth Factor beta
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pubmed:year |
1999
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pubmed:articleTitle |
Expression of insulin-like growth factor binding protein-3 (IGFBP-3) in human keratinocytes is regulated by EGF and TGFbeta1.
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pubmed:affiliation |
Centre for Hormone Research, Royal Children's Hospital, Parkville, Victoria, Australia.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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