Like all tissues in the body, the eye needs a healthy blood supply to function properly. Poorly developed or damaged blood vessels can lead to visual impairment or even blindness. This is commonly seen in diseases such as diabetic retinopathy, vascular occlusions such as central retinal venous occlusion (CRVO) and Branch retinal venous occlusion (BRVO) (click here for more information about CRVO or BRVO), etc. While many of the molecules involved in guiding the development of the intricate blood vessel architecture are known, only now are the scienitists learning how these molecules work, and more importantly, how they affect sight.
Reporting in the Oct. 16 issue of Cell, researchers at the Johns Hopkins School of Medicine in Baltimore, Maryland, US, find that when some cells in the mouse retina are not properly fed by blood vessels, they can yet remain alive for many months and can later recover some or all of their normal function, suggesting that similar conditions in people may also be reversible.
Three genes -- named Fz4, Ndp and Lrp5 -- previously were suspected to be involved in blood vessel development in the human retina. Defects in any of these genes cause hypovascularization -- a lack of sufficient blood vessels -- in the retina. Similarly, eliminating any of these genes in mice can lead to hypovascularized retinas.
Mice lacking functional Fz4 have poor blood vessel growth in the retina and are blind, but it was not known whether the blood vessel deficiency was the cause of blindness or whether the absence of Fz4 leads to some other defect that causes blindness. The team found that Fz4 function is required only in blood vessels, where it senses a signal produced by the Ndp gene in other retinal cells.
When the team measured electrical responses in retinal cells of mice lacking Fz4, they found a defect in electrical signaling in the middle layer of the retina -- the same region lacking blood vessels.
The researchers then bathed the Fz4 mutant retinas in oxygen and nutrients to mimic a normal blood supply, and measured electrical signaling in response to light. They found that when provided with oxygen and nutrients, the retinas were able to sense light and generate signals similar to those generated by normal retinas. The team suggests that in the absence of Fz4 the defective blood vessels provide the retinas with only enough oxygen and nutrients to keep the retinal cells alive, but not enough for them to function normally to send electrical signals.
Since these experiments have not been tried in humans, it is difficult to say what may happen when such experiements are undertaken some time later. But if the human retina responds to a decrease in blood supply in the same way that the mouse retina has been seen to have responded, then these results may have a significant relevance for those patients with vision loss due to vascular damage, such as diabetic retinopathy and vascular occlusions.
No comments:
Post a Comment