Differential expression of fibroblast growth factor‐2 and fibroblast growth factor receptor 1 in a scarring and nonscarring model of CNS injury in the rat
Differential expression of fibroblast growth factor‐2 and fibroblast growth factor receptor 1 in a scarring and nonscarring model of CNS injury in the rat
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大鼠中枢神经系统损伤疤痕和非疤痕模型中成纤维细胞生长因子-2和成纤维细胞生长因子受体1的差异表达
DOI:
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发表时间:
2001
影响因子:
3.4
通讯作者:
A. Logan
中科院分区:
文献类型:
--
作者:
Conrad S. Smith;M. Berry;Wendy E. Clarke;A. Logan
Injury to the adult brain results in abortive axon regeneration and the deposition of a dense fibrous glial scar. Therapeutic strategies to promote postinjury axon regeneration are likely to require antiscarring strategies. In neonatal brain wounds, scar material is not laid down and axons grow across the lesion site, either by de novo growth or regeneration. To achieve the therapeutic goal of recapitulating the nonscarring neonatal response in the injured adult, an understanding of how ontogenic differences in scarring reflect developmental diversities in the trophic response to injury is required. Fibrobast growth factor‐2 (FGF‐2) expression is developmentally regulated and has been implicated as a regulator of the wounding response of the adult rat central nervous system. We have investigated the expression of FGF‐2 and fibroblast growth factor receptor 1 (FGFR1) after penetrating lesions to the cerebral cortex of 5 days post partum (dpp) (nonscarring) and 16 dpp and adult (scarring) rats. In situ hybridization, immunohistochemistry and Western blotting showed robust and sustained increases in FGF‐2 and FGFR1 mRNA and protein in reactive astrocytes around the lesion in scarring rats, a response that was attenuated substantially in the nonscarring neonate. These results demonstrate that changes in astrocyte FGF‐2 and FGFR1 expression are coincident with the establishment of a mature pattern of glial scarring after injury in the maturing central nervous system, but it is premature to infer a causal relationship without further experiments.
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影响因子:
--
作者:
Daniel E. Johnson;L. Williams
通讯作者:
Daniel E. Johnson;L. Williams
DOI:
10.1073/pnas.83.9.3012
发表时间:
1986
影响因子:
11.1
作者:
Walicke,P;Cowan,WM;Ueno,N;Baird,A;Guillemin,R
通讯作者:
Guillemin,R
影响因子:
15.9
作者:
Montero, A;Okada, Y;Hurley, MM
通讯作者:
Hurley, MM
DOI:
10.1016/0165-3806(90)90240-y
发表时间:
1990-03-01
期刊:
DEVELOPMENTAL BRAIN RESEARCH
影响因子:
--
作者:
CADAY, CG;KLAGSBRUN, M;FINKLESTEIN, SP
通讯作者:
FINKLESTEIN, SP
影响因子:
3.4
作者:
LOGAN, A;BERRY, M;BAIRD, A
通讯作者:
BAIRD, A