Abstract
Although morphological changes in microglia have been reported to be associated with diabetic retinopathy, little is known about the early changes in the microglia and macrophages during the progression of this condition. The present study was aimed at characterizing retinal microglial activation in the early stages of experimental diabetic retinopathy. Toward this end, a model of diabetic retinopathy was generated by intraperitoneally injecting male Sprague-Dawley rats with streptozotocin. No apparent histological changes were observed during the early stages of experimental diabetic retinopathy. However, at 4 to 16 weeks after the onset of diabetes, the retinas from diabetic rats exhibited higher density of microglia than those from age-matched normal controls, with microglial density peaking at 12 weeks. In particular, the proportion of the activated microglia increased significantly in the diabetic rats, specifically in the nerve fiber and ganglion cell layers, whereas it decreased in the inner plexiform layer within 12 weeks. Furthermore, the resident retinal microglial cells were activated immediately after diabetes induction, peaked at 12 weeks, and remained for up to 16 weeks after disease onset. Thus, experimental diabetic retinopathy causes gradual hypoxia and neuroinflammation, followed by the activation of microglia and the migration of macrophages. The distribution and density of retinal microglial activation changed typically with the progression of the disease in early-stage diabetic rats.
Highlights
Diabetic retinopathy (DR) is a major complication of diabetes and a leading cause of blindness, with the severe form of the disease affecting the working-age population on a global scale [1, 2]
All procedures performed in studies involving animals were in accordance with the ethical standards of the Institutional Animal Care and Use Committee (IACUC) and Department of Laboratory Animals (DOLA) in the Catholic University of Korea where the studies were conducted
Iba-1+ cells were mainly distributed in the inner layers of the retina, and most microglia exhibited a ramified morphology
Summary
Diabetic retinopathy (DR) is a major complication of diabetes and a leading cause of blindness, with the severe form of the disease affecting the working-age population on a global scale [1, 2]. Current accepted pharmacological treatments for DR including diabetic macular edema are intravitreal antivascular endothelial growth factor (VEGF) or steroids [3, 4] They are administered by intravitreal injection and stabilize the detrimental effects of VEGF on microvascular proliferation and permeability [5]. Lazzara et al reported a dysregulation in the expression of several miRNAs in diabetic mice and displayed their ability to be potent mediators in the pathological mechanisms associated with DR [6, 7]. These can reveal miRNAgene-pathways that are modulated in the early phase of DR and other microvascular diseases
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