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A. A. Veenstra, T. Kern; Microglial Infiltration into the Retina of Diabetic Mice. Invest. Ophthalmol. Vis. Sci. 2009;50(13):5897.
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Early abnormalities in diabetic retinopathy (DR) are consistent with chronic subclinical inflammation. Diabetic mice lacking either ICAM-1 or CD18 have decreased vascular leakage and capillary degradation, suggesting that leukocyte infiltration or adhesion may play an important role.
To evaluate which leukocytes might be migrating into the diabetic retina we transplanted bone marrow from mice expressing green fluorescent protein (GFP) into wild type diabetic mice. We adapted widefield imaging and immuno-histochemistry techniques to identify and quantitate marrow derived cells in retinal flat mounts.
After eight months of diabetes the only GFP+ / CD45+ cells present in the retina of diabetic mice were microglia (based on cell shape and immunolabeling). The number of GFP+ cells in the retina was similar in diabetic and non diabetic mice. The number of "resident" non GFP microglia between the inner nuclear layer (INL) and outer nuclear layer (ONL) decreased by approximately one half compared to nondiabetic controls while those in the ganglion cell layer (GCL) and INL were similar to nondiabetic litermates.
These studies do not confirm findings in diabetic rats, (where increases in the number of microglia have been reported), but demonstrate a loss of microglia from the retina of diabetic mice.
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