| First Author | Jungnickel J | Year | 2004 |
| Journal | Mol Cell Neurosci | Volume | 25 |
| Issue | 3 | Pages | 444-52 |
| PubMed ID | 15033172 | Mgi Jnum | J:89373 |
| Mgi Id | MGI:3040001 | Doi | 10.1016/j.mcn.2003.11.007 |
| Citation | Jungnickel J, et al. (2004) Targeted disruption of the FGF-2 gene affects the response to peripheral nerve injury. Mol Cell Neurosci 25(3):444-52 |
| abstractText | Basic fibroblast growth factor (FGF-2) is involved in the development, maintenance, and survival of the nervous system. To study the physiological role of endogenous FGF-2 during peripheral nerve regeneration, we analyzed sciatic nerves of FGF-2-deleted mice by using morphometric, morphological, and immunocytochemical methods. Quantification of number and size of myelinated axons in intact sciatic nerves revealed no difference between wild-type and FGF-2 knock-out (ko) animals. One week after nerve crush, FGF-2 ko mice showed about five times more regenerated myelinated axons with increased myelin and axon diameter in comparison to wild-types close to the injury site. In addition, quantitative distribution of macrophages and collapsed myelin profiles suggested faster Wallerian degeneration in FGF-2-deleted mice close to the lesion site. Our results suggest that endogenous FGF-2 is crucially involved in the early phase of peripheral nerve regeneration possibly by regulation of Schwann cell differentiation. |
