Linked Life Data

12914536

Source:http://linkedlifedata.com/resource/pubmed/id/12914536

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2003-8-13
pubmed:abstractText
The mouse mammary epithelial cell line HC11 upregulates the synthesis of beta-casein (a differentiation marker) following treatment with the lactogenic hormone mix dexamethasone, insulin and prolactin (DIP). We demonstrate that the basal levels of IGF-binding protein (IGFBP)-5 secreted by undifferentiated HC11 cells are upregulated 10-fold during DIP-induced cellular differentiation whereas the level of the other IGFBP species secreted by HC11 cells (IGFBP-2) is downregulated during this process. As previously reported, the combination of all three of these hormones is required for synthesis of the differentiation marker beta-casein, whereas basal IGFBP-5 secretion is evident in the absence of any hormonal treatment and, unlike beta-casein, secretion of this protein can be stimulated by binary combinations of the hormones (although maximal levels of IGFBP-5 are achieved in the presence of all three lactogenic hormones). Additionally, levels of IGFBP-5 can be increased by DIP treatment under conditions (non-competency of HC11 cultures or presence of epidermal growth factor) where DIP treatment does not increase synthesis of beta-casein. For IGFBP-2, dexamethasone is a potent inhibitor of secretion whilst prolactin stimulated the secretion of this binding protein into the medium. For the IGFBP axis in HC11 cells we conclude that, although the levels of IGFBP-5 and -2 are influenced by the state of cellular differentiation, the hormonal regulation of the levels of these IGFBP species can be dissociated from the regulation of beta-casein synthesis. In a further series of experiments we demonstrate that IGF-I is able to replace insulin in the DIP lactogenic hormone mix and by the use of a specific IGF-I receptor blocking antibody indicate that the action of IGF-I is mediated through the cell surface IGF-I receptor and not by cross-reaction of IGF-I ligand at the insulin receptor. We discuss our data in the context of the potential role of the IGF axis in the process of cell differentiation and illustrate the significance of our findings in the context of the physiology and life cycle of the mammary epithelial cell.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0952-5041
pubmed:author
pubmed:issnType
Print
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
197-208
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Hormonal control of IGF-binding protein (IGFBP)-5 and IGFBP-2 secretion during differentiation of the HC11 mouse mammary epithelial cell line.
pubmed:affiliation
Molecular Recognition Group, Hannah Research Institute, Ayr KA6 5HL, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't