TY  - JOUR
A1  - Kiprianova, Irina
A1  - Schindowski, Katharina
A1  - Bohlen und Halbach, Oliver von
A1  - Krause, Sonja
A1  - Dono, Rosanna
A1  - Schwaninger, Markus
A1  - Unsicker, Klaus
T1  - Enlarged infarct volume and loss of BDNF mRNA induction following brain ischemia in mice lacking FGF-2
T2  - Experimental neurology
N2  - FGF-2, a potent multifunctional and neurotrophic growth factor, is widely expressed in the brain and upregulated in cerebral ischemia. Previous studies have shown that intraventricularly or systemically administered FGF-2 reduces the size of cerebral infarcts. Whether endogenous FGF-2 is beneficial for the outcome of cerebral ischemia has not been investigated. We have used mice with a null mutation of the fgf2 gene to explore the relevance of endogenous FGF-2 in brain ischemia. Focal cerebral ischemia was produced by occlusion of the middle cerebral artery (MCAO). We found a 75% increase in infarct volume in fgf2 knock-out mice versus wild type littermates (P < 0.05). This difference in the extent of ischemic damage was observed after 24 h, and correlated with decreased viability in fgf2 mutant mice following MCA occlusion. Increased infarct volume in fgf2 null mice was associated with a loss of induction in hippocampal BDNF and trkB mRNA expression. These findings indicate that signaling through trkB may contribute to ameliorating brain damage following ischemia and that bdnf and trkB may be target genes of FGF-2. Together, our data provide the first evidence that endogenous FGF-2 is important in coping with ischemic brain damage suggesting fgf2 as one crucial target gene for new therapeutic strategies in brain ischemia.
KW  - Cerebral ischemia
KW  - FGF-2 KO
KW  - BDNF
KW  - trkB
KW  - Hippocampus
KW  - Parietal cortex
Y1  - 2006
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/1972
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30-34407
SN  - 1090-2430
SN  - 0014-4886
N1  - Copyright © 2004 Elsevier Inc. All rights reserved.
VL  - 189
IS  - 2
SP  - 252
EP  - 260
PB  - Elsevier ; Academic Press
CY  - Amsterdam [u. a.] ; Orlando, Fla.
ER  -