eye disease

Molecule that regulates blood vessels in the eye could help with diabetic retinopathy

by Barbara Hewitt on March 27, 2017

The identification of a new molecule that induces the formation of abnormal blood vessels in the eye could help prevent vision damage in people with diabetes.

Diabetic retinopathy caused by changes in the vasculature of people with diabetes can cause long term complications and affects about 93 million people across the world.

But researchers at the Bascom Palmer Eye Institute, part of the University of Miami Miller School of Medicine, have identified a new molecule that induces the formation of abnormal blood vessels in the eyes of diabetic mice.

The study suggests that inhibiting this molecule may prevent similarly aberrant blood vessels from damaging the vision of not only diabetics, but also premature infants.

Many people with diabetic retinopathy suffer a dramatic loss of vision as the blood vessels supplying the retina become leaky and new, abnormal blood vessels are formed to replace them.

A molecule called vascular endothelial growth factor (VEGF) regulates blood vessel growth and leakiness, and two VEGF inhibitors, ranibizumab (Lucentis) and aflibercept (Eylea), have been approved to treat retinal vascular leakage, though they are only successful in about a third of patients.

Study lead author Wei Li, a research associate professor of ophthalmology, and his colleagues at Bascom Palmer developed a technique called comparative ligandomics to identify additional molecules that regulate the behaviour of blood vessels in diabetic mice.

The approach allows the researchers to compare the signalling molecules that selectively bind to the surface of retinal blood vessel cells in diabetic but not healthy animals.

‘It is estimated that between one-third and a half of all marketed drugs act by binding to cell surface signalling molecules or their receptors. Our ligandomics approach can be applied to any type of cell or disease to efficiently identify signalling molecules with pathogenic roles and therapeutic potential,’ said Li.

Using this technique the researchers discovered that a protein called secretogranin III (Scg3) efficiently binds to the surface of retinal blood vessel cells in diabetic, but not healthy, mice.

Although Scg3 promotes the secretion of hormones and other signalling factors, it wasn’t thought to have a signalling function itself. Nevertheless, the researchers found that Scg3 increased vascular leakage, and, when administered to mice, it stimulated blood vessel growth in diabetic animals, but not in healthy mice.

VEGF, in contrast, stimulates blood vessel growth in both diabetic and healthy mice. Li and colleagues think that Scg3 binds to a distinct cell surface receptor that is specifically up-regulated in diabetes.

Treating diabetic mice with Scg3-neutralizing antibodies dramatically reduced the leakiness of their retinal blood vessels. Moreover, the antibodies significantly inhibited the growth of new blood vessels in mice with oxygen-induced retinopathy, a well-established animal model of human retinopathy of prematurity.

Though the researchers still need to confirm the role of Scg3 in humans, they believe that inhibiting this protein could be an effective treatment for both diabetic retinopathy and ROP, especially as it appears to have no role in normal vascular development.

‘Scg3 inhibitors may offer advantages such as disease selectivity, high efficacy, and minimal side effects. Because they target a distinct signalling pathway, anti-Scg3 therapies could be used in combination with, or as an alternative to, VEGF inhibitors,’ Li said.

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