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.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.