Linked Life Data

15013107

Source:http://linkedlifedata.com/resource/pubmed/id/15013107

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-3-11
pubmed:abstractText
Insulin-like growth factor-I (IGF-I) is an important anabolic growth factor in the maintenance of articular cartilage phenotypic expression. Chondrocyte morphology is also tightly linked to phenotype. The small G-protein Cdc42 plays a key role in regulation of cell morphology and phenotypic expression in several cell types and, we show here, in articular chondrocytes. The purpose of these studies was to investigate possible links between the intracellular signaling pathways of IGF-I and Cdc42 in articular chondrocytes. Treatment of chondrocytes with IGF-I resulted in a rapid and sustained decrease in the activation state (decreased GTP-bound) of Cdc42. Nucleotide exchange and hydrolysis experiments suggest that the decreased activation occurs through increased hydrolysis. Transient expression of dominant-negative Cdc42(T17N) allowed for enhanced expression of normal chondrocyte phenotype as determined by increased mRNA expression of collagen type II (Coll II) with decreased matrix metalloproteinase-3 (MMP-3) expression. The results of these studies suggest a novel link between IGF-I and Cdc42 signaling pathways. Further, an additional mechanism for the regulation of chondrocyte phenotype is defined through the IGF-I induced down-regulation of Cdc42 activation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0736-0266
pubmed:author
pubmed:issnType
Print
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
436-45
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Insulin-like growth factor-I diminishes the activation status and expression of the small GTPase Cdc42 in articular chondrocytes.
pubmed:affiliation
Department of Clinical Sciences, Cornell University, Ithaca, NY 14853, USA. laf4@cornell.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.