Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1997-5-27
pubmed:abstractText
In a recent report, we demonstrated that intracerebral injections of the pleiotropic cytokine, ciliary neurotrophic factor (CNTF), into developing postnatal rats evoked a severe inflammatory response as determined by the appearance of reactive astrocytes and activated microglia. Considering the likely involvement of CNTF in the injury response, we felt it was important to further understand the role of CNTF in the developing rat CNS. In this study, we examined the responsiveness of other cell populations to intracerebral injections of CNTF. We report that CNTF increases glial fibrillary acidic protein (GFAP), while having no appreciable effect on the levels of other intermediate filaments including vimentin and neurofilament. Moreover, CNTF did not affect the expression of the mature oligodendrocyte gene, myelin basic protein. These results suggest that CNTF is highly specific in its regulation of GFAP. In our previous study, we showed CNTF to increase GFAP in a cell population that already exists in the CNS parenchyma. To determine the origin of the CNTF-induced reactive astrocytes, therefore, we have utilized a technique of combined in situ hybridization and immunocytochemistry. To examine the possibility that CNTF acts on oligodendrocyte precursors to give rise to reactive astrocytes, the platelet-derived growth factor alpha receptor (PDGF-alpha R) was utilized as a riboprobe in conjunction with an antibody to GFAP. Examination of CNTF-induced GFAP+ astrocytes revealed no colocalization with PDGF-alpha R mRNA. In contrast, when we utilized an S100 alpha antibody recognizing a calcium binding protein in immature astrocytes, we found colocalization of S100 alpha and GFAP mRNA. These data suggest that CNTF induces an upregulation of GFAP in immature S100 alpha + astrocytes. Examination of the CNTF-alpha receptor mRNA revealed no change in expression following CNTF treatment. Unexpectedly, however, the CNTF-induced astrogliotic response appears to be indirect since the CNTF-alpha receptor was solely expressed by neurons in the cytokine-treated animals.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0165-3806
pubmed:author
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
98
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
221-33
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:9051264-Animals, pubmed-meshheading:9051264-Astrocytes, pubmed-meshheading:9051264-Biological Markers, pubmed-meshheading:9051264-Brain, pubmed-meshheading:9051264-Ciliary Neurotrophic Factor, pubmed-meshheading:9051264-Female, pubmed-meshheading:9051264-Gene Expression Regulation, pubmed-meshheading:9051264-Glial Fibrillary Acidic Protein, pubmed-meshheading:9051264-Male, pubmed-meshheading:9051264-Microglia, pubmed-meshheading:9051264-Nerve Growth Factors, pubmed-meshheading:9051264-Nerve Tissue Proteins, pubmed-meshheading:9051264-Phenotype, pubmed-meshheading:9051264-Rats, pubmed-meshheading:9051264-Rats, Wistar, pubmed-meshheading:9051264-Receptor, Ciliary Neurotrophic Factor, pubmed-meshheading:9051264-Receptors, Nerve Growth Factor, pubmed-meshheading:9051264-Recombinant Proteins, pubmed-meshheading:9051264-S100 Proteins, pubmed-meshheading:9051264-Stem Cells
pubmed:year
1997
pubmed:articleTitle
CNTF induces GFAP in a S-100 alpha brain cell population: the pattern of CNTF-alpha R suggests an indirect mode of action.
pubmed:affiliation
Department of Neurobiology, UCLA, School of Medicine 90024-1764, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't