Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1994-2-18
pubmed:abstractText
Nerve growth factor (NGF) promotes survival and maintenance of peripheral and central neurons. In previous studies, we found that low-affinity NGF binding sites were associated with flat nonneuronal cells dissociated and cultured from the embryonic septum. These cells were also labeled with a monoclonal antibody to the NGF receptor, 192 IgG, suggesting that low-affinity NGF receptors are associated with a nonneuronal population. To define the potential effect of NGF on these nonneuronal cells, rat Embryonic Day 17 (E17) septa were dissociated and cultured in fully defined medium in the presence of NGF. Glial fibrillary acidic protein (GFAP) was used as a marker for the astrocyte population. NGF elicited a dramatic ninefold increase in the number of GFAP-positive cells after 7 days. NGF similarly increased astrocyte number in cultures grown from E18 hippocampi and E16 substantia nigra, suggesting that NGF acts on glia from multiple brain regions. To begin defining the mechanism of NGF action on astrocytes, we examined [3H]thymidine incorporation, which increased significantly, but by only 50%, upon exposure to the trophic factor. We tentatively conclude that NGF increases astrocyte number in culture by stimulating mitosis as well as enhancing survival or differentiation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0014-4886
pubmed:author
pubmed:issnType
Print
pubmed:volume
124
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
377-80
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
NGF increases brain astrocyte number in culture.
pubmed:affiliation
Department of Neurology, Cornell University Medical College, New York, New York 10021.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S.