Abstract:
Bi-directional communication between axon and Schwann cell is vital to the peripheral nervous system (PNS) myelination process. Disruption of this highly regulated communication is the main underlying reason of peripheral neuropathies. Understanding the molecular mechanism of this interaction is important to unravel the pathology of these diseases. Previous studies performed in our laboratory demonstrated that FGF1 is localized to axons, whereas FGF receptors are localized to Schwann cells, similar to that of NRG1 that is the most well-known protein acting in this interaction. Moreover, in vitro studies have shown that FGF1 may have a possible role during PNS myelination. Thus, in this study, we aimed to further investigate the possible role of FGF1 and its receptors (FGFR1-3) during PNS myelination process through in vivo experiments. For this purpose, we used mouse sciatic nerve as an in vivo model of PNS and used PNS remyelination procedure in which lysolecithin-induced demyelination promotes a remyelination period that mimick developmental myelination. Initially, we determined the time points for demyelinationremyelination processes through immunohistochemistry and western blotting. Secondly, we blocked FGF1 and its receptors one by one during remyelination period and investigated their effect on remyelination via western blot analysis. The results of this study further demonstrated that FGF1 has a possible role during PNS myelination process, but probably in an intracrine manner. Together with the studies previously performed in our laboratory, this study provides evidence for the involvement of FGF1 in PNS myelination process that has not been demonstrated previously in the literature.
