Purpose. To determine if the expression of fibroblast growth factor receptors (FGF-R) are altered in a mouse model of oxygen-induced retinopathy. Methods. Postnatal day 7 C57BL/6 mice were exposed to 75% O2 for 5 days (P12 O2) then recovered in room air for an additional 9 days (P21 O2). Immunohistochemistry was used to examine the expression of FGF-R1 (flg) and FGF-R2 (bek) in hyperoxia-exposed mouse eyes as well as room air controls on P12 & P21. Results. FGF-R1 immunostaining was present in ganglion cells and inner nuclear layer (INL) cells on P12 and P21 in both control and O2 exposed eyes. Müller cell processes were also labeled in the P12 control and O2 eyes. Neovascular tufts which extended into the vitreous in P21 O2 eyes were positive for FGF-R1, FGF-R2 was localized along the inner limiting membrane (ILM) and outer plexiform layer (OPL) in P12 control eyes. Moderate immunostaining was seen in Müller cell processes located in the inner plexiform layer (IPL) in P12 O2 eyes. On P21 the FGF-R2 staining continued to be localized along the ILM and OPL. In contrast, the P21 O2 eyes exhibited intense immunostaining in the nerve fiber layer, the Müller cell processes in the IPL & OPL, the retinal vessels, and the neovascular tufts. Conclusions. Müller cells and retinal endothelial cells respond with increased expression of FGF-R2 in this model of retinopathy. Both FGF receptors were localized in neovascular tufts in the oxygen-injured eyes. Altered expression of FGF receptors in this model suggests a possible role for fibroblast growth factors in oxygen-induced neonatal eye injury.
|Original language||English (US)|
|Journal||Investigative Ophthalmology and Visual Science|
|State||Published - Feb 15 1996|
ASJC Scopus subject areas
- Sensory Systems
- Cellular and Molecular Neuroscience