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Alexander A Veenstra, Timothy Kern; Role of Inflammatory CCR2+ Monocytes in Early Stage Diabetic Retinopathy. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1050.
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© ARVO (1962-2015); The Authors (2016-present)
Previous work demonstrated that neutrophils and perhaps monocytes play a critical role in diabetes-induced vascular lesions of the retina observed in the early stages of diabetic retinopathy. Previous attempts to create monocyte deficient animals with MCSFR-/- bone marrow were not successful in diabetic animals. Animals deficient in CCR2 do not release a sub population of “inflammatory” monocytes into the blood resulting in a monocyte deficient phenotype.
Experimental diabetes was induced in mice with streptozotocin. Diabetes-induced retinal vascular loss, leukostasis, retinal superoxide production and leukocyte activation were evaluated at durations of up to 8 months diabetes in mice lacking CCR2 and WT controls.
Mice deficient in CCR2 exhibited significantly reduced diabetes-induced degeneration of retinal capillaries , leukostasis, and superoxide production. Leukocytes isolated from diabetic CCR2-/- mice exhibited reduced superoxide production and a decreased capacity to kill mouse retinal endothelial cells when co-cultured in vitro.
Inflammatory monocytes contribute to leukocyte mediated degeneration of retinal capillaries in diabetes, and this is mediated at least in part by CCR2
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