Triggering Mechanism For Diabetic Retinopathy Found

A mechanism explaining the onset of diabetic retinopathy was found by researchers at Case Western Reserve University School of Medicine.

The investigators determined that receptor proteins called CD40 on the surface of Muller cells in the retina instigate harmful inflammation, leading to vision impairment. Identifying these cells gives researchers a target for treating retinopathy, one of the more debilitating complications of diabetes.

The receptor CD40 is found on cells throughout the body, and earlier research showed that mice with no CD40s were protected from diabetic retinopathy. So, the research team created mice that only had CD40 on their retinas’ Muller cells to learn more about this receptor.

It was discovered that CD40 causes Muller cells to secrete ATP, a tiny energy molecule. The ATP then triggers an inflammatory response in nearby microglia and macrophage cells. This mechanism is sufficient to cause the damaging inflammation associated with retinopathy.

Retinopathy impairs the retina’s capacity to sense light. Though scientists have long suspected inflammation was behind this disease, it was difficult to sort through the variety of retinal cells and signal molecules involved.

“The choice of Muller cells was not obvious since it would have been logical to predict that CD40...on microglia, macrophages, or endothelial cells would have been the major driver of inflammation in the retina,” said researcher Carlos Subauste, M.D. However, the culprit turned out to be CD40 on the surface of Muller cells, which in turn activates the other cell types.

Because CD40 is present throughout the body, the research also suggests this receptor might be implicated in other inflammatory illnesses such as atherosclerosis, lupus, or certain bowel diseases.

Currently, Subauste and colleagues are experimenting with drug interventions that block CD40 induced inflammation in mice. Their goal is to prevent diabetic retinopathy.

Source: Science Daily

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