In the PNS, this neurite outgrowth continues. In CNS, however, it stops for several reasons. Most important are the neurite inhibitory effect of the exposed Nogo’s on the surface of the injured oligodendrocytes, the relative lack of enhanced growth factor production by injured glia in the injured area, and the cavitation and the scar tissue formation induced by the inflammatory reaction (Steward et al. Inhibitors,research,lifescience,medical 1999; Norenberg

et al. 2004; Profyris et al. 2004). There is a distinct difference in production and availability of growth factors in CNS for multiple reasons. Part of SCI-research has therefore come to focus on growth factors as medical “primers” of the injured spinal cord. There are a number of growth factors that have been shown

to alter different cell types and functions, reducing the deleterious effects of an injury, while improving neuronal survival and regeneration. FGF2, which is present in both neurons and glial cells, has previously been reported to have multiple neural-promoting effects on the developing and the adult nervous system Inhibitors,research,lifescience,medical of mice and other mammals. FGF2 has also been found to play an important role in inducing and regulating the this website proliferation of neural stem cells and precursors, Inhibitors,research,lifescience,medical promoting their survival and maintenance in vitro (Arsenijevic et al. 2001; Mudò et al. 2009). This mitogenic effect was also detected on spinal cord-derived neural precursors (Ray and Gage 1994). With proper induction

and expansion, cultures of neural precursors were able to survive, proliferate, and migrate after engraftment at the site of SCI (Karimi-Abdolrezaee et al. 2006). FGF2 also plays a role in regulating the proliferative fate and differentiation of unipotent (neuronal) and bipotent (neuronal/astroglial) Inhibitors,research,lifescience,medical mouse-derived neural precursor cells, and hence, the generation of neurons and astrocytes in the developing CNS (Vescovi et al. 1993). After administration of neutralizing antibodies against endogenous Inhibitors,research,lifescience,medical FGF2 (Tao et al. 1997), significant depression of the rate of neural proliferation and development, was seen. In mice next models, FGF2 was found to reduce inflammation by decreasing multiple inflammatory cells and markers such as macrophages, microglia, CD8 T-cells (Ruffini et al. 2001; Rottlaender et al. 2011), and limited the CD44-mediated leukocyte migration (Jones et al. 2000). Contradictory results have been shown on its effect on astrocytosis and gliosis (Reilly et al. 1998; Goddard et al. 2002; Kasai et al. 2010). However, an interesting observation in zebra fish was that maturing astrocytes exhibited long bipolar processes, which bridged across the two sides of the injured spinal cord. These glial bridges were found to play a role as routes for axonal growth during regenerative neurogenesis, and its formation was dependent on the presence of FGF-signaling (Goldshmit et al. 2012).