Accumulation of advanced glycation end products potentiate human retinal capillary endothelial cells mediated diabetic retinopathy
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- Published online on: August 20, 2019 https://doi.org/10.3892/mmr.2019.10590
- Pages: 3719-3727
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Copyright: © Tao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
The major ophthalmic complication in patients with diabetes is diabetic retinopathy (DR), which is one of the major eye diseases that causes blindness. It is well established that the occurrence and duration of DR is positively correlated with duration of diabetes. Advanced glycation end product (AGE) accumulation in patients with diabetes is one factor that leads to the development of DR. However, the underlying mechanisms remain unclear. In the present study, the role of phosphoinositide 3‑kinase/protein kinase B (Akt) signaling in AGE‑induced DR development was investigated. An in vitro experimental system was used to study the effects of AGEs on human retinal capillary endothelial cells (HRCECs) and Müller cells. Flow cytometry, MTT, western blotting and BrdU incorporation assays were performed. Reverse transcription‑quantitative polymerase chain reaction was used to measure the expression of angiogenesis‑associated genes. Functional assays of angiogenesis, including HRCEC invasion and tube formation assays. It was demonstrated that the expression of receptor for AGEs was upregulated in HRCECs and Müller cells following treatment with AGEs. AGE treatment did not affect Müller cell viability, but enhanced HRCEC viability. Akt inhibition increased cell apoptosis and death in HRCECs. AGE treatment upregulated the expression of pro‑angiogenic genes, which was suppressed by Akt inhibitor treatment. In addition, Akt inhibitor treatment suppressed HRCEC invasion and tube formation ability. The present study suggested that Akt‑mediated signaling may serve critical roles in the development of DR due to the accumulation of AGEs. Akt may be a potential therapeutic target in DR.
