Expression of fibroblast growth factor-2 and fibroblast growth factor receptor 1 messenger RNAs in spinal ganglia and sciatic nerve: regulation after peripheral nerve lesion
Section snippets
Animal surgery
Experiments were performed on adult female Hanover–Wistar rats (Charles River Wiga, Sulzfeld, Germany) weighing approximately 180 g. For surgery, animals were anaesthetized intraperitoneally using sodium pentobarbital (50 mg/kg). The left sciatic nerve was exposed and crushed with a fine forceps at the mid-thigh level. After survival intervals, from one to 28 days (d), animals were killed and L4–L6 DRG ipsilateral and contralateral to the lesion were collected. Sciatic nerve segments extending 8
Expression of FGF-2 and FGF receptor 1 in intact spinal ganglia and sciatic nerve
FGF-2 and FGFR1 transcripts were constitutively expressed in spinal ganglia and sciatic nerve.
In spinal ganglia FGF-2 mRNA was localized to satellite cells as shown by in situ hybridization. Almost all of the satellite cells were labelled (Figs 1, 2). FGFR1 displayed a neuronal localization in DRG, most of the neurons showed the signal albeit at different intensities (Fig. 1Fig. 2). Using ribonuclease protection assay expression of both transcripts FGF-2 and FGFR1 was also found in intact DRG (
Discussion
In the present study we demonstrate for the first time, that FGF-2 and FGFR1 mRNAs are constitutively expressed in spinal ganglia and sciatic nerve of the adult rat. Furthermore, we show that after crush lesion of the sciatic nerve expression of FGF-2 is increased in both the proximal and distal stump and in the DRG whereas the level of FGFR1 mRNA is exclusively increased in the lesioned sciatic nerve. This different spatial regulation of FGF-2 and FGFR1 argues for a diverse, region-specific
Conclusion
The presence and up-regulation after injury of FGF-2 and FGFR1 mRNAs in sensory ganglia and in the peripheral nerve suggests that FGF-2 is involved in regeneration phenomena of the peripheral nervous system. In DRG FGF-2 could mediate survival promoting activity or other, non-trophic functions. At the lesion side FGF-2 could help to control the onset and rate of myelination in regenerating nerves.
Acknowledgements
We thank Dr A. Baird for kindly providing the FGF-2 cDNA and Dr J. Milbrandt for the FGFR-1 cDNA. We also thank C. Zeschnigk, H. Arnold, and C. Micucci for excellent technical assistance and help in preparing the figures and Dr S. Wewetzer for reading of the manuscript. This work was supported by Deutsche Forschungsgemeinschaft (SFB 505/TPA2).
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