BASIC FIBROBLAST GROWTH-FACTOR EXPRESSION AND TENASCIN-C IMMUNOREACTIVITY AFTER PARTIAL UNILATERAL HEMITRANSECTION OF THE RAT-BRAIN

Citation
A. Lippoldt et al., BASIC FIBROBLAST GROWTH-FACTOR EXPRESSION AND TENASCIN-C IMMUNOREACTIVITY AFTER PARTIAL UNILATERAL HEMITRANSECTION OF THE RAT-BRAIN, Brain research, 730(1-2), 1996, pp. 1-16
Citations number
69
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
730
Issue
1-2
Year of publication
1996
Pages
1 - 16
Database
ISI
SICI code
0006-8993(1996)730:1-2<1:BFGEAT>2.0.ZU;2-V
Abstract
Basic fibroblast growth factor (bFGF) gene expression as well as its i mmunoreactivity were studied after partial unilateral hemitransection of the rat brain during a time course of 24 h, 72 h, 7 and 14 days. Th e mechanical injury resulted in a global increase of bFGF gene express ion at the 24-h time interval. This global increase was seen at the ip silateral site at the level of the lesion as well as rostral to the le sion in the ipsilateral hemisphere. The upregulation in bFGF gene expr ession was in most of the areas investigated due to an upregulation in glial cells as seen by means of nonradioactive in situ hybridization compared with immunocytochemistry for glial fibrillary acidic protein (GFAP). Basic FGF immunoreactivity (IR) was increased around the lesio n in glial cell nuclei 7 days after the injury. This increase was also detected in GFAP positive glial cells surrounding small vessels in th e lesioned area. Moreover, in the present paper we demonstrate increas ed tenascin immunoreactivity in the lesioned area 7 days after injury. The tenascin IR was increased at the edges of the lesion as well as i n vessel like structures. The tenascin IR was partially codistributed with GFAP IR in the lesioned area. The lesion was also characterized b y an increase in vimentin IR as well as in laminin IR. It is suggested that the observed changes in the expression of bFGF, matrix proteins (laminin, tenascin) and intermediate filaments (vimentin) are involved in (a) tissue repair, (b) protection of neuronal cells from excitotox ic influences and (c) formation of new Vessels in the lesioned area.