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Aging increases retinal vascular lesions characteristic of early diabetic retinopathy

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Abstract

The goal of this study was to determine whether aging induces retinal vascular lesions that are similar to those seen in diabetic retinopathy. Female rats were randomly divided into four groups; each group represented a time point and consisted of four non-diabetic rats and four diabetic rats. At time points of 3, 12, 18, or 22 months of age, retinas were isolated and subjected to retinal trypsin digestion (RTD) for isolation of retinal capillary networks. Blood glucose, body weight, and hemoglobin A1c (HbA1c) levels were monitored throughout the study. One RTD from each animal was stained with Hematoxylin and Periodic Acid Schiff’s (PAS) reagent to analyze acellular capillaries and pericyte loss, while the contralateral RTD from each animal was subjected to TUNEL assay to assess apoptosis in the retinal vascular cells. The numbers of acellular capillaries and pericyte loss were significantly increased between the 12 vs. 18 month groups, and the 18 vs. 22 month groups. Similarly, acellular capillaries and pericyte loss increased with aging in the diabetic rat retinas; however, the appearance of acellular capillaries and pericyte loss occurred at 3 months of diabetes. TUNEL assay showed increased apoptosis associated with acellular capillaries and pericyte loss in both normal, aged rats and diabetic rats. In conclusion, retinal vascular lesions that develop in aged rat retinas have striking similarities to those of diabetic rat retinas. The breakdown of normal vascular architecture with aging appears to have resemblance with the anatomical and histological lesions associated with diabetic retinopathy.

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Acknowledgments

Research was supported by NEI, NIH EY014702 (SR) and NIA, NIH AG025049 (JT), and in part by a departmental grant from the Massachusetts Lions Organization (SR).

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Correspondence to Sayon Roy.

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Roy, S., Tonkiss, J. & Roy, S. Aging increases retinal vascular lesions characteristic of early diabetic retinopathy. Biogerontology 11, 447–455 (2010). https://doi.org/10.1007/s10522-010-9263-x

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  • DOI: https://doi.org/10.1007/s10522-010-9263-x

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