Autophagy dysregulation mediates the damage of high glucose to retinal pigment epithelium cells
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Rong Li. Department of Ophthalmology, the First Affiliated Hospital of Xi’an Medical University, Xi’an 710077, Shaanxi Province, China. Rechelrong198222@163.com

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Supported by National Natural Science Foundation of China (No.82070973); Key Research and Development Plan of Shaanxi Province (No.2021SF-157).

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    Abstract:

    AIM: To observe the role and mechanism of autophagy in retinal pigment epithelial cell (RPE) damaged by high glucose, so as to offer a new idea for the treatment of diabetic retinopathy (DR). METHODS: ARPE-19, a human RPE cell line cultured in vitro was divided into the normal control (NC), autophagy inhibitor 3-methyladenine (3-MA), high-glucose (HG), and HG+3-MA groups. Cell viability was detected by CCK-8 assay and the apoptosis rate was measured by flow cytometry. The protein expressions of apoptosis markers, including Bax, Bcl-2, and Caspase-3, as well as autophagy marker including microtubule-related protein 1 light chain 3 (LC3), p62, and mechanistic target of rapamycin (mTOR) were detected by Western blotting. Autophagic flux was detected by transfection with Ad-mCherry-GFP-LC3B. RESULTS: Under high glucose conditions, the viability of ARPE-19 was decreased, and the apoptosis rate increased, the protein expressions of Bax, Caspase-3, and LC3-II/LC3-I were all increased and the expressions of Bcl-2, p62 and p-mTOR decreased, and autophagic flux was increased compared with that of the controls. Treatment with 3-MA reversed all these changes caused by high glucose. CONCLUSION: The current study demonstrates the mechanisms of cell damage of ARPE-19 through high glucose/mTOR/autophagy/apoptosis pathway, and new strategies for DR may be developed based on autophagy regulation to manage cell death of RPE cells.

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Qian Zhang, Hong-Song Li, Rong Li, et al. Autophagy dysregulation mediates the damage of high glucose to retinal pigment epithelium cells. Int J Ophthalmol, 2021,14(6):805-811

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Publication History
  • Received:September 28,2020
  • Revised:February 25,2021
  • Adopted:
  • Online: April 23,2021
  • Published: