Effect of intranasal administration of basic fibroblast growth factor on olfactory epithelium

Abstract

To further study the effects of basic fibroblast growth factor (bFGF) on the olfactory epithelium, bFGF was intranasally administered twice a day for 6 weeks to 2.5-month-old and 7-month-old mice. The effects were immunohistochemically examined by using antibodies against proliferating cell nuclear antigen, olfactory marker protein, and GAP43. The number of cells positive for proliferating cell nuclear antigen in the supporting cell layer increased dramatically, and that of GAP43-positive cells, or globose basal cells, increased significantly, especially in aging mice. However, no significant changes were observed in the number of olfactory marker protein-positive cells or mature olfactory receptor neurons. These results suggest that topical application of bFGF promotes proliferation of globose basal cells and supporting cells.

Treatment of Neural Anosmia by Topical Application of Basic Fibroblast Growth Factor–Gelatin Hydrogel in the Nasal Cavity

“…The results were markedly different. The latter effectively promoted recovery from neural anosmia, whereas the former had only a small beneficial effect, as reported by Nishikawa et al 8 Gelatin hydrogel is biologically inactive and is considered to be ineffective in terms of recovery from damage. 21 These effects are likely due to sustained release of bFGF, as the hydrogel degrades slowly in the body.…”

Neuropeptide Y and extracellular signal-regulated kinase mediate injury-induced neuroregeneration in mouse olfactory epithelium

“…Surprisely, the number of BrdU+ cells in the ATP+NPY-instilled group was significantly (p < 0.05) reduced when compared to NPY-instilled group, suggesting that instillation of ATP with NPY may compromise NPY-induced increases in basal cell proliferation. To further examine the potential synergism of ATP and polypeptide growth factors in OE neuroregeneration, we used FGF2 that has been shown to promote GBC proliferation in the OE in vivo (Nishikawa et al, 2009) and in vitro (Newman et al, 2000). Our recent data indicate that FGF2 is released following ATP application and is partially responsible for the ATP-induced increase in OE neuroregeneration (Jia et al, 2011a).…”

“…We chose NPY and FGF2 to investigate this hypothesis as both NPY Y1 and FGF2 receptors are expressed in basal cells (Hansel et al, 2001; Hsu et al, 2001). Further, NPY activation of Y1 receptors increases phospho-p44/42 ERK and basal cell proliferation (Hansel et al, 2001) and FGF2 stimulates the proliferation of GBCs in vitro (Barraud et al, 2007; Goldstein et al, 1997; Newman et al, 2000) and in vivo (Nishikawa et al, 2009). In the CNS, FGF2 promotes cell proliferation through activation of p44/42 ERK signalling (Neary et al, 2008) and ATP potentiates the mitogenic effect of FGF2 by parallel activation of p44/42 ERK via P2 purinergic receptors (Grimm et al, 2009; Neary et al, 2005; Neary et al, 1996).…”

ATP differentially upregulates fibroblast growth factor 2 and transforming growth factor alpha in neonatal and adult mice: effect on neuroproliferation

“…FGF2 stimulates the proliferation of globose basal cells in adult in vivo (Nishikawa et al, 2009) and in vitro (Newman et al, 2000), and in postnatal OE cell cultures (Barraud et al, 2007) and cell lines (Goldstein et al, 1997). In addition, FGF2 is released (Ensoli et al, 1998) and stimulates the proliferation of progenitor cells in embryonic cell cultures (DeHamer et al, 1994, Ensoli et al, 1998).…”