Hyperglycemia Activates Retinal Photoreceptors to Induce Neuroglial Inflammation
Abstract Diabetic retinopathy (DR) is a major cause of vision loss in working-age adults. Accumulating evidence suggests that retinal photoreceptors contribute to the initiation and progression of diabetic retinopathy. In this study, we investigated whether hyperglycemia directly alters photoreceptor signaling and whether photoreceptor-derived inflammatory mediators activate downstream Muller…
Diabetic retinopathy, a leading cause of vision loss among working-age adults, appears to be influenced by hyperglycemia, according to a recent study. Researchers isolated primary photoreceptors from adult mice and cultured them with normal glucose, high D-glucose, or high L-glucose, using high L-glucose as an osmotic control. They analyzed the conditioned media of the photoreceptors for inflammatory and growth factors, and then used these media to stimulate primary Müller glia.
The results showed that high glucose exposure led to an increase in photoreceptor production of TNF-a, IL-6, and VEGF. Furthermore, conditioned media from high glucose-treated photoreceptors induced the expression of IL-1b, TNF-a, and IL-6 in Müller glia. These Müller glia exposed to photoreceptor-conditioned media also showed increased expression and secretion of VEGF, as well as enhanced expression, secretion, and gelatinase activity of MMP-9.
The study concludes that photoreceptors act as glucose-responsive neuronal cells that can trigger and bolster neuroglial inflammatory signaling in hyperglycemic conditions.
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