Study Finds Lack Of The Protein, VEGF, Can Cause Defects Similar To Dry Macular Degeneration
November 11, 2009
Adapted from the Schepens Eye Research Institute
Scientists at Schepens Eye Research Institute have found that when the eye is missing a form of vascular endothelial growth factor (VEGF) that when secreted can reach other cells at a distance, the retina shows defects similar to "dry" macular degeneration. This finding, published in the November 3, 2009 print edition of PNAS (Proceedings of the National Academy of Sciences), not only increases the understanding of the causes of this blinding disease, but it may also impact the use of anti-VEGF drugs, such as Lucentis, which are designed to neutralize VEGF in eyes with "wet" macular degeneration.
"These results are significant for several reasons. We know little about what causes [dry macular degeneration] or how to treat it. Our discovery may be an important piece of the puzzle. It shows that reduced VEGF [leads to degeneration of one of the layers in the retina]. Therefore, the continuous blockage of VEGF may contribute to the development of or a worsening of [the dry form of the disease]," says Patricia D'Amore, principal investigator of the study and senior scientist at Schepens.
VEGF is a protein that stimulates the growth of new blood vessels. The eye produces several different forms of VEGF that differ in their size and their ability to move away from the producing cell.
Age-related macular degeneration (AMD) is a disease that destroys the macula, the central part of the retina responsible for detailed vision needed for reading, driving and face recognition. It comes in two types—"wet" and "dry." In wet AMD, a pathological overproduction of VEGF leads to the development of abnormal blood vessels, which leak and damage the retina. Wet AMD can be treated with some success with anti-VEGF drugs that block abnormal blood vessel growth and leakage. Dry macular degeneration develops less rapidly, and is related to an accumulation of debris under the retina.
Knowing that one of the retinal layers in the adult produces VEGF, the Schepens team hypothesized that in a healthy individual ,this layer produces forms of VEGF that, when secreted, can move away and reach another layer to support its function and survival.
In the PNAS study, the researchers tested their hypothesis using a genetic mouse model in which the one of the retinal layers produced a form of VEGF that was unable to reach other retinal cells at a distance. As the mice aged, they began to display an age-dependent degeneration of both the retina, culminating with the death of photoreceptors and vision loss, similar to that observed in dry macular degeneration.
The next step in the research, according to the first author Dr. Magali Saint-Geniez, is to determine if this model can be used to design new therapies.
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