Scientists eye molecular target for AMD

Researchers in the US have discovered a key role for the STAT3 protein in both mouse and human tissue, offering hope of a new molecular target for treatment

18 Aug 2015 by Ryan O'Hare

A signalling molecule which activates white blood cells in the eye could offer a new treatment target for patients with wet age-related macular degeneration (AMD), according to new research.

Previous research had shown that, before vision loss occurs, levels of an anti-inflammatory signalling molecule called interleukin-10 (IL-10) increase in the eye. The numbers of a specific type of white blood cell, M2 macrophages, also increase, which ultimately contributes to the formation of abnormal blood vessels characteristic of wet AMD. However, the link between the two was unclear. 

By engineering mice with various IL-10 signalling pathways disabled, researchers at Washington University in the US found that one of the pathways, involving a particular protein called STAT3, was interacting with immune cells in the eye. STAT3 activated and altered the macrophages and ultimately resulted in the formation of the abnormal blood vessels. 

High levels of the same protein were also found in human retina tissue samples from wet AMD patients treated in previous decades. The findings offer hope that compounds used to disrupt the action of STAT3 in mice could be used in patients with wet AMD. 

Principle researcher, Dr Rajendra S. Apte, a professor of ophthalmology and visual science at the university’s School of Medicine, said: “When we inhibit this pathway, we can alter the immune cells and interfere with abnormal blood vessel growth in mice. Doing so might open therapeutic avenues to halt vision loss or even restore sight in people who have macular degeneration.” 

He added: “Now that we have a better idea of how these macrophages are activated at the molecular level, we may be able to use those drugs to halt or reverse the process.” 

The research is published in the journal Nature Communications.

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