Linked Life Data

10679766

Source:http://linkedlifedata.com/resource/pubmed/id/10679766

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2000-3-16
pubmed:abstractText
Multipotent neural progenitor cells become progressively more biased towards a glial fate during development coincident with an increase in expression of the epidermal growth factor receptor (EGFR). To determine whether differences in lineage commitment of neural progenitor cells from different stages are causally related to expression of the EGFR and whether generation of glia is EGFR-dependent, we used an EGFR-specific tyrosine kinase inhibitor, PD158780, to block the activation of EGFR in progenitor cells. Treatment of cultured neonatal progenitor cells with PD158780 completely blocked EGF-induced proliferation of the cells but did not affect bFGF-induced proliferation. Nevertheless, treatment with the inhibitor failed to inhibit the generation of astroglia in the presence of either EGF or bFGF. Treatment with bone morphogenetic protein-2 (BMP2) enhanced astroglial differentiation and suppressed oligodendroglial (OL) differentiation. PD158780 treatment had no effect on the BMP2-induced astroglial differentiation or OL suppression. These observations suggest that the generation of astroglia is not dependent on EGFR activation. Because it was still possible that the progenitor cell responses reflected a prior history of EGFR signaling, rat forebrain cells were cultured in the presence of PD158780 from a time (E12.5) preceding expression of the EGFR. After time in culture, the E12.5 cells expressed EGFR by Western analysis both in the presence and in the absence of PD158780, but activation of EGFR kinase (receptor autophosphorylation) was undetectable in the presence of PD158780 and the cells did not proliferate in response to EGF. Nevertheless, astroglial differentiation was normal in PD158780-treated cells both in the absence and in the presence of BMPs or CNTF. Furthermore, the propensity towards glial differentiation increased with time in culture even in the absence of EGFR signaling. This suggests that the increased bias towards glial differentiation during development does not depend on EGFR signaling.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0360-4012
pubmed:author
pubmed:copyrightInfo
Copyright 2000 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
59
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
312-20
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Developmental changes in neural progenitor cell lineage commitment do not depend on epidermal growth factor receptor signaling.
pubmed:affiliation
Departments of Neurology and Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't