Diabetic retinopathy (DR) is a complication of diabetes, caused by high blood sugar levels damaging the retinal microvasculature. Mechanisms, such as oxidative stress and deposition of advanced glycation end products, leads to glial cell activation and neuronal apoptosis. Pericytes, contractile cells that wrap around vascular endothelial cells play a central role in blood-retinal barrier function are targeted in DR. Somatostatin (SST) is an important neuroprotective molecule synthesised in the retina. It is anti-angiogenic and inhibits apoptotic activity in photoreceptor cells. SST is downregulated in DR and administration of exogenous SST is protective. In this paper a microglia cell line BV2, was challenged with lipopolysaccharide (LPS), SST or both, and conditioned media was collected. Human retinal pericytes treated with LPS media showed a significant increase in proinflammatory (TNF) and pro-apoptotic factors (FasL and caspase-8). SST inhibited the effects of LPS challenge and increased survival of pericytes. These results show that SST is able to mediate microglial-induced inflammation in the retina and protect pericytes in the early stages of DR. 

Somatostatin protects retinal pericytes from inflammation mediated by microglia.
Mazzeo A, Arroba AI, Beltramo E, et al.
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Graham Wallace

Birmingham and Midland Eye Centre, Birmingham, UK.

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