| Registro completo |
| Provedor de dados: |
BJMBR
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| País: |
Brazil
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| Título: |
Analysis of trophic responses in lesioned brain: focus on basic fibroblast growth factor mechanisms
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| Autores: |
Chadi,G.
Fuxe,K.
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| Data: |
1998-02-01
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| Ano: |
1998
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| Palavras-chave: |
Radioautography
In situ hybridization
Basic fibroblast growth factor
FGF receptor
Astrocyte
Image analysis
Central nervous system
Brain lesion
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| Resumo: |
The actions of fibroblast growth factors (FGFs), particularly the basic form (bFGF), have been described in a large number of cells and include mitogenicity, angiogenicity and wound repair. The present review discusses the presence of the bFGF protein and messenger RNA as well as the presence of the FGF receptor messenger RNA in the rodent brain by means of semiquantitative radioactive in situ hybridization in combination with immunohistochemistry. Chemical and mechanical injuries to the brain trigger a reduction in neurotransmitter synthesis and neuronal death which are accompanied by astroglial reaction. The altered synthesis of bFGF following brain lesions or stimulation was analyzed. Lesions of the central nervous system trigger bFGF gene expression by neurons and/or activated astrocytes, depending on the type of lesion and time post-manipulation. The changes in bFGF messenger RNA are frequently accompanied by a subsequent increase of bFGF immunoreactivity in astrocytes in the lesioned pathway. The reactive astrocytes and injured neurons synthesize increased amount of bFGF, which may act as a paracrine/autocrine factor, protecting neurons from death and also stimulating neuronal plasticity and tissue repair
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| Tipo: |
Info:eu-repo/semantics/article
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| Idioma: |
Inglês
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| Identificador: |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1998000200007
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| Editor: |
Associação Brasileira de Divulgação Científica
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| Relação: |
10.1590/S0100-879X1998000200007
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| Formato: |
text/html
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| Fonte: |
Brazilian Journal of Medical and Biological Research v.31 n.2 1998
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| Direitos: |
info:eu-repo/semantics/openAccess
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