Premium
The role of FGF2 in the in vitro proliferation and angiogenesis of human choroidal endothelial cells
Author(s) -
STEWART EA,
AMOAKU WMK
Publication year - 2008
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2008.412.x
Subject(s) - angiogenesis , matrigel , macular degeneration , vascular endothelial growth factor , intracellular , blot , growth factor , microbiology and biotechnology , cancer research , medicine , fibroblast growth factor , vascular endothelial growth factor a , biology , immunology , ophthalmology , vegf receptors , receptor , genetics , gene
Purpose Age‐related macular degeneration (AMD) is the most common cause of irreversible visual loss in elderly populations in the western world. The mechanism of this disease is not yet fully understood, although vascular endothelial growth factor (VEGF) is thought to be the most significant growth factor in AMD, other growth factors, including FGF2 also stimulates the proliferation of human choroidal endothelial cells (hCEC). These factors may explain the only partial success of current anti‐VEGF AMD treatments. Methods hCEC were isolated from cadaver eyes and cultured in EBM2‐MV medium as previously published. hCEC proliferation after exposure to VEGF and FGF2 was measured using the WST‐1 assay and angiogenesis assessed using a double layer Matrigel technique. Western blotting was used to examine the intracellular signalling stimulated by FGF2 and VEGF. Results hCEC proliferation was increased in response to both FGF2 and VEGF. This effect was cumulative, indicating that these work through different intracellular signalling pathways. Western blotting identified common and differential intracellular signalling between the two growth factors. Conclusion Currently VEGF is thought to be the most important growth factor which stimulates neovascularisation leading to AMD and treatments developed reflect this. However, these results show that FGF2 also stimulates neovascularisation and may play a role in AMD development. A treatment which targets downstream signalling common to both growth factors may provide a more targeted and therefore successful treatment.