Mice lacking basic fibroblast growth factor showed faster sensory recovery.
Neurotrophic factors have been shown to stimulate and support peripheral nerve repair. One of these factors is basic fibroblast growth factor (FGF-2), which is up-regulated after peripheral nerve injury and influences early sciatic nerve regeneration by regulating Schwann cell proliferation. Our previous study on FGF-2 deficient mice indicated that FGF-2 is important for axonal maturation and remyelination one week after sciatic nerve crush (Jungnickel, J., Claus, P., Gransalke, K., Timmer, M. and Grothe, C., 2004. Targeted disruption of the FGF-2 gene affects the response to peripheral nerve injury. Mol. Cell. Neurosci. 25, 444-452). However, the functional impact of these effects on sensory and motor fibers was not clear. After performing pinch test, walking track analysis and rotarod, we found faster recovery of mechanosensory but not of motor function in mutant mice. To elucidate the role of FGF-2 on structural recovery, we analyzed FGF-2 deficient mice and wild-type littermates 2 and 4 weeks after sciatic nerve crush. Two weeks after peripheral nerve injury, regenerating fibers of mutant mice showed both significantly increased axon and myelin size, but no difference in the number of myelinated and unmyelinated fibers. Molecular analysis indicated that the expression level of myelin protein zero was significantly enhanced in lesioned nerves in the absence of FGF-2. These results suggest that loss of FGF-2 could positively influence restoration of mechanosensory function by accelerating structural recovery transiently.
Jungnickel
Julia
J
Hannover Medical School, Institute of Neuroanatomy, Germany. jungnickel.julia@mh-hannover.de
Haastert
Kirsten
K
Grzybek
Martin
M
Thau
Nadine
N
Lipokatic-Takacs
Esther
E
Ratzka
Andreas
A
Nölle
Anna
A
Claus
Peter
P
Grothe
Claudia
C
D000818:Animals; D004195:Disease Models, Animal; D016222:Fibroblast Growth Factor 2 / Q000172:deficiency*; D005786:Gene Expression Regulation / Q000235:genetics; D008124:Locomotion / Q000235:genetics*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D046529:Microscopy, Electron, Transmission / Q000379:methods; D004676:Myelin Basic Protein / Q000235:genetics / Q000378:metabolism; D018993:Myelin P0 Protein / Q000235:genetics / Q000378:metabolism; D009186:Myelin Sheath / Q000378:metabolism; D009416:Nerve Regeneration / Q000235:genetics*; D011597:Psychomotor Performance / Q000502:physiology; D012333:RNA, Messenger / Q000378:metabolism; D020127:Recovery of Function / Q000235:genetics*; D045442:Rotarod Performance Test / Q000379:methods; D012583:Schwann Cells / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D020426:Sciatic Neuropathy / Q000473:pathology / Q000503:physiopathology*; D011984:Sensory Receptor Cells / Q000473:pathology / Q000502:physiology* / Q000648:ultrastructure
D004676:Myelin Basic Protein; D018993:Myelin P0 Protein; D012333:RNA, Messenger; D016222:Fibroblast Growth Factor 2