Vascular endothelial growth factor and ocular neovascularization.

JW Miller - The American journal of pathology, 1997 - ncbi.nlm.nih.gov
The American journal of pathology, 1997ncbi.nlm.nih.gov
Okamoto et al have developed an extremely useful and interesting model of retinal and
subretinal neovascularization. Using molecular techniques, they have developed a
transgenic model driven by overexpression of VEGF, a growth factor demonstrated to play
an important role in neovascularization in many ocular diseases. They have been able to
demonstrate that VEGF overexpression is sufficient to cause intraretinal and subretinal
neovascularization. The mouse model is relatively cheap and reliable, does not require any …
Abstract
Okamoto et al have developed an extremely useful and interesting model of retinal and subretinal neovascularization. Using molecular techniques, they have developed a transgenic model driven by overexpression of VEGF, a growth factor demonstrated to play an important role in neovascularization in many ocular diseases. They have been able to demonstrate that VEGF overexpression is sufficient to cause intraretinal and subretinal neovascularization. The mouse model is relatively cheap and reliable, does not require any exogenous agent, and has many characteristics of clinical intraocular neovascularization. The new vessels develop in the outer retina and subretinal space and have a characteristic histological appearance. They leak fluorescein on angiography, demonstrating their similarity to human disease and allowing identification and grading of neovascularization in vivo. The model can be used to investigate molecular mechanisms of VEGF-dependent neovascularization, with applications beyond ocular eye disease. The model can also be used to study anti-angiogenic agents that have the potential to treat common blinding diseases such as age-related macular degeneration. Okamoto et al have made a substantial contribution to the angiogenesis field with this work, and one looks forward to future investigations.
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