Linked Life Data

17395707

Source:http://linkedlifedata.com/resource/pubmed/id/17395707

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2007-6-18
pubmed:abstractText
Of the many factors that regulate linear growth, IGF-I has a central role in epiphyseal chondrocyte development. Whether IGF-I is solely of systemic or also of local origin is uncertain, as is how other growth factors interact with IGF-I at the growth plate. We studied the proliferative effects of IGF-I on juvenile bovine epiphyseal chondrocytes fractionated by density gradient centrifugation. Cell density correlated with size, glycogen content, and gene expression patterns. There was a gradient of response to IGF-I, with the greatest proliferative response in high-density cells corresponding to the reserve zone, as measured by [3H]thymidine uptake. Low-density (hypertrophic zone) cells proliferated only when exposed to IGF-I and basic fibroblast growth factor (FGF). The gradient of IGF-I response correlated with [125I]IGF-I binding as determined by Scatchard analysis: IGF-I receptor number was 10-fold greater in reserve zone cells than in hypertrophic cells. When exposed to basic FGF for 24 hours, IGF-I binding in hypertrophic cells increased 3-fold. In contrast, no specific binding of GH was demonstrated in juvenile bovine chondrocytes. GH produced neither signal transducer and activator of transcription phosphorylation, increased proliferation, nor increased IGF-I mRNA levels in any chondrocyte fraction. IGF-I mRNA levels were extremely low at 800-1100 copies/microg 18S RNA in bovine chondrocytes. These results suggest that the major regulator of chondrocyte proliferation is systemic IGF-I; FGFs may influence the actions of IGF-I at the growth plate by altering its receptor number in chondrocytes.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
148
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3122-30
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:17395707-Animals, pubmed-meshheading:17395707-Binding, Competitive, pubmed-meshheading:17395707-Binding Sites, pubmed-meshheading:17395707-Blotting, Western, pubmed-meshheading:17395707-Cattle, pubmed-meshheading:17395707-Cell Proliferation, pubmed-meshheading:17395707-Cell Survival, pubmed-meshheading:17395707-Cells, Cultured, pubmed-meshheading:17395707-Chondrocytes, pubmed-meshheading:17395707-Collagen Type II, pubmed-meshheading:17395707-Fibroblast Growth Factors, pubmed-meshheading:17395707-Growth Hormone, pubmed-meshheading:17395707-Growth Plate, pubmed-meshheading:17395707-Hedgehog Proteins, pubmed-meshheading:17395707-Humans, pubmed-meshheading:17395707-Insulin-Like Growth Factor I, pubmed-meshheading:17395707-Male, pubmed-meshheading:17395707-Phosphorylation, pubmed-meshheading:17395707-Receptor, IGF Type 1, pubmed-meshheading:17395707-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:17395707-STAT5 Transcription Factor, pubmed-meshheading:17395707-Somatomedins, pubmed-meshheading:17395707-Swine
pubmed:year
2007
pubmed:articleTitle
Insulin-like growth factor-I and fibroblast growth factor, but not growth hormone, affect growth plate chondrocyte proliferation.
pubmed:affiliation
Division of Pediatric Endocrinology, Department of Pediatrics, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9063, USA. michele.hutchison@utsouthwestern.edu
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural