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ShareMay 19, 2008 — In the industrialized world, most diseases that cause vision loss do so by altering the permeability of the blood vessels in the retina of the eye such that fluid accumulates in the retina impairing eyesight.
For many of these diseases, the molecule VEGF is the initiator of increased blood vessel permeability and recent clinical data have indicated that VEGF antagonists can stabilize, or even improve, the eyesight of some patients.
However, such treatment requires repeated injection of the VEGF antagonist into the eye.
A potentially more painless and simple approach to reducing VEGF-induced blood vessel permeability in the eye has now been suggested by the work of Martin Friedlander and colleagues, at The Scripps Institute, La Jolla, in mouse and rabbit models of increased VEGF-mediated blood vessel permeability.
In the study, a small molecule inhibitor of the signaling molecules that associate with the receptors of VEGF (which are known as Src kinases) was found to eliminate VEGF-induced accumulation of fluid in the retina of mice and rabbits.
This effect was observed both when the inhibitor was injected intravenously and when the inhibitor was administered in an eye drop. The specificity of the approach was confirmed by showing that the inhibitor did not prevent VEGF-induced accumulation of fluid in the retina of mice lacking the Src kinases that associate with the receptor of VEGF.
The authors therefore suggest that future studies should investigate whether this approach would be of benefit to individuals with the many diseases that cause vision loss through VEGF-induced increased blood vessel permeability.
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The above story is reprinted from materials provided by Journal of Clinical Investigation, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Retinal vascular permeability suppression by topical application of a novel VEGFR2/Src kinase inhibitor in mice and rabbits. Journal of Clinical Investigation, May 15, 2008.
Note: If no author is given, the source is cited instead.
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