Linked Life Data

8869596

Source:http://linkedlifedata.com/resource/pubmed/id/8869596

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1996-12-2
pubmed:abstractText
We have previously shown that the response of osteoblasts to parathyroid hormone (PTH) can be influenced at the receptor level by growth on the physiological substrate, type I collagen, or by treatment with retinoic acid. We have also shown differential expression of genes when cells of the osteoblast lineage are grown on type I collagen. The aim of this study was therefore to examine the effect of retinoic acid and growth on type I collagen on PTH/PTH-related protein (PTHrP) receptor mRNA expression in the osteosarcoma osteoblast-like cell line UMR 106-06. PTH/PTHrP receptor mRNA levels, as assessed by Northern blot, of cells grown on collagen were increased up to 2-fold compared with cells on plastic and in a concentration-dependent manner with respect to collagen. An increase was seen as early as 6 h and was maintained over a 24 h period. This was not due to increased mRNA stability. Retinoic acid decreased the level of receptor mRNA on both plastic and collagen at each time but did not alter mRNA stability. For all treatments PTH/PTHrP receptor mRNA abundance, relative to glyceraldehyde-3-phosphate dehydrogenase, increased steadily over 24 h after subculture of cells. In contrast, PTHrP mRNA levels were reduced in cells on collagen, compared with plastic. PTH-stimulated cAMP levels of cells grown on collagen were increased compared with plastic at 24 h, but not earlier. Consistent with the mRNA data, retinoic acid decreased the amplitude of cAMP responses in cells on plastic and collagen. There was no evidence for changes in adenylate cyclase per se, since forskolin-induced cAMP levels did not change with either treatment. This study shows that known modulators of osteoblast maturation also affect signal transduction in these cells by regulating gene expression of the PTH/PTHrP receptor as well as the PTHrP ligand.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-0795
pubmed:author
pubmed:issnType
Print
pubmed:volume
150
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
299-308
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8869596-Animals, pubmed-meshheading:8869596-Blotting, Northern, pubmed-meshheading:8869596-Cell Line, pubmed-meshheading:8869596-Collagen, pubmed-meshheading:8869596-Cyclic AMP, pubmed-meshheading:8869596-Electrophoresis, Agar Gel, pubmed-meshheading:8869596-Forskolin, pubmed-meshheading:8869596-Gene Expression, pubmed-meshheading:8869596-Oligonucleotide Probes, pubmed-meshheading:8869596-Osteoblasts, pubmed-meshheading:8869596-Parathyroid Hormone, pubmed-meshheading:8869596-Parathyroid Hormone-Related Protein, pubmed-meshheading:8869596-Polymerase Chain Reaction, pubmed-meshheading:8869596-Proteins, pubmed-meshheading:8869596-RNA, Messenger, pubmed-meshheading:8869596-Rats, pubmed-meshheading:8869596-Receptor, Parathyroid Hormone, Type 1, pubmed-meshheading:8869596-Receptors, Parathyroid Hormone, pubmed-meshheading:8869596-Tretinoin
pubmed:year
1996
pubmed:articleTitle
A type I collagen substrate increases PTH/PTHrP receptor mRNA expression and suppresses PTHrP mRNA expression in UMR106-06 osteoblast-like cells.
pubmed:affiliation
St Vincent's Institute of Medical Research, Fitzroy, Victoria, Australia.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't