Linked Life Data

16093398

Source:http://linkedlifedata.com/resource/pubmed/id/16093398

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
32
pubmed:dateCreated
2005-8-11
pubmed:abstractText
Fibroblast growth factors (FGFs) have been implicated in numerous cellular processes, including proliferation, migration, differentiation, and survival. Whereas FGF-2, the prototypic ligand in a family of 22 members, activates all four tyrosine kinase FGF receptors (FGFR1-FGFR4), other members demonstrate a higher degree of selectivity. Oligodendrocytes (OLs), the myelin-producing cells of the CNS, are highly influenced by FGF-2 at all stages of their development. However, how other FGFs and their cognate receptors orchestrate the development of OLs is essentially undefined. Using a combination of specific FGF ligands and receptor blocking antibodies, we now show that FGF-8 and FGF-17 target OL progenitors, inhibiting their terminal differentiation via the activation of FGFR3, whereas FGF-9 specifically targets differentiated OLs, triggering increases in process growth via FGFR2 signaling; FGF-18 targets both OL progenitors and OLs via activation of both FGFR2 and FGFR3. These events are highly correlated with changes in FGF receptor expression from FGFR3 to FGFR2 as OL progenitors differentiate into mature OLs. In addition, we demonstrate that, although activation of FGFR1 by FGF-2 leads to proliferation of OL progenitors, it produces deleterious effects on differentiated OLs (i.e., aberrant reentry into cell cycle and down-regulation of myelin proteins with a loss of myelin membrane). These data suggest that ligand availability, coupled with changes in FGF receptor expression, yield a changing repertoire of ligand-receptor signaling complexes that contribute critically to the regulation of both normal OL development and potential OL/myelin pathogenesis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
10
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7470-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:16093398-Animals, pubmed-meshheading:16093398-Cell Aging, pubmed-meshheading:16093398-Cell Differentiation, pubmed-meshheading:16093398-Cell Lineage, pubmed-meshheading:16093398-Cell Proliferation, pubmed-meshheading:16093398-Cells, Cultured, pubmed-meshheading:16093398-Fibroblast Growth Factors, pubmed-meshheading:16093398-Myelin Sheath, pubmed-meshheading:16093398-Oligodendroglia, pubmed-meshheading:16093398-Protein Isoforms, pubmed-meshheading:16093398-Rats, pubmed-meshheading:16093398-Receptor, Fibroblast Growth Factor, Type 1, pubmed-meshheading:16093398-Receptor, Fibroblast Growth Factor, Type 2, pubmed-meshheading:16093398-Receptor, Fibroblast Growth Factor, Type 3, pubmed-meshheading:16093398-Receptors, Fibroblast Growth Factor, pubmed-meshheading:16093398-Signal Transduction, pubmed-meshheading:16093398-Stem Cells
pubmed:year
2005
pubmed:articleTitle
Distinct fibroblast growth factor (FGF)/FGF receptor signaling pairs initiate diverse cellular responses in the oligodendrocyte lineage.
pubmed:affiliation
Department of Neuroscience, University of Connecticut Medical School, Farmington, Connecticut 06030, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, N.I.H., Extramural