ALTERATIONS IN FIBROBLAST GROWTH-FACTOR RECEPTOR EXPRESSION FOLLOWINGBRAIN INJURY

Citation
Jf. Reilly et Vg. Kumari, ALTERATIONS IN FIBROBLAST GROWTH-FACTOR RECEPTOR EXPRESSION FOLLOWINGBRAIN INJURY, Experimental neurology, 140(2), 1996, pp. 139-150
Citations number
52
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00144886
Volume
140
Issue
2
Year of publication
1996
Pages
139 - 150
Database
ISI
SICI code
0014-4886(1996)140:2<139:AIFGRE>2.0.ZU;2-R
Abstract
Traumatic injuries to the central nervous system result in astrogliosi s and the formation of a dense scar at the site of the wound. Basic fi broblast growth factor (bFGF) has mitogenic and morphogenic effects on astrocytes, and an interaction between bFGF and its receptor is likel y to play a role in astrogliosis. We examined trauma-induced changes i n the spatial and temporal expression of FGF receptor (FGFR) in adult rats over a 28-day period following a stereotaxic lesion through the c ortex and hippocampus. Immunohistochemistry and image analysis were us ed to evaluate the changes. Antibody characterization studies strongly suggested that staining represented FGFR 1, but did not rule out poss ible cross-reactivity with FGFR 2 or 3. Double immunohistochemistry fo r FGFR and glial fibrillary acidic protein demonstrated that mature as trocytes expressed FGFR. Expression was increased on astrocytes adjace nt to the wound cavity by Day 2 postlesion. Staining increased further through Day 10 and decreased to control values by Day 28, except for a sustained increase in staining of reactive astrocytes immediately ad jacent to the wound cavity. Basic FGF was detected in the nuclei of ce lls staining for FGFR, suggesting that FGFR-expressing astrocytes also contained bFGF. These data demonstrate a time course for astrocyte ex pression of FGFR that precedes and parallels the time course for astro cyte hypertrophy. Our observations suggest that endogenous bFGF, actin g directly on FGFR-expressing astrocytes, may contribute to astroglios is. (C) 1996 Academic Press, Inc.