Purpose. Basic fihroblast growth factor (bFGF) has been suggested to play an important role in retinal neovascularization (NV). This study was designed to determine if bFGF is necessary to produce retinal NV in a murine model of oxygeninduced ischémie retinopathy. Methods. Targeted mutation of the bFGF gene was introduced into mice by homologous recombination. Mice homozygous for the hFGF gene distruption were viable, appeared normal, and were fertile. At postnatal day 7 (P7), bFGF -I- mice and bFGF +/+ control mice with the same genetic background were placed in a 75% oxygen environment for 5 days, followed by room air for 5 days, and then sacrified. Eyes were enucleated and frozen sections were stained with the endothelial specific marker griffonia simpliciforia lectin I isolectin B4. Retinal vascular area was quantitated by image analysis. Results, The retinas, including the vasculature, of untreated P17 hFGF -I- mice appeared normal by light microscopy. All bFGF -I- and bFGF +/+ mice with ischémie retinopathy had retinal NV. Retinal vascular area was 48882.0 ±1639.7 nm:/ section in bFGF -I- mice (n=4) and was not statistically different from that in bFGF +1+ mice which was 47407.3 ±648.8 |im2/ section (n=7). Conclusions. Mice deficient in bFGF develop retinal NV to the same extent as wild type mice in a model of ischémie retinopathy, suggesting that either bFGF does not play a role in the development of retinal NV or ihere is complete complemention by another growth factor.
|Original language||English (US)|
|Journal||Investigative Ophthalmology and Visual Science|
|State||Published - Dec 1 1997|
ASJC Scopus subject areas
- Sensory Systems
- Cellular and Molecular Neuroscience