Long noncoding RNA TPTEP1 suppresses diabetic retinopathy by reducing oxidative stress and targeting the miR-489-3p/NRF2 axis

  • Xinfa Wang Department of Ophthalmology, The First People’s Hospital of Lin’an District, Hangzhou City, Zhejiang Province 311300, China
  • Xianbo Zhou Department of Ophthalmology, The First People’s Hospital of Lin’an District, Hangzhou City, Zhejiang Province 311300, China
  • Fang Wang Department of Nephrology, General Hospital of Central Theater Command of PLA, Wuhan City, Hubei Province 430010, China
  • Nan Zhang Department of Ophthalmology, The First People’s Hospital of Lin’an District, Hangzhou City, Zhejiang Province 311300, China
  • Yan Zhang Department of Ophthalmology, The Seventh Medical Center of the PLA General Hospital, Haidian District, Beijing 100700, China
  • Zhen Ao Department of Ophthalmology, The Eighth Medical Center of the PLA General Hospital, Haidian District, Beijing 100091, China
  • Fang He Department of Ophthalmology, The Eighth Medical Center of the PLA General Hospital, Haidian District, Beijing 100091, China
DOI: https://doi.org/10.18388/abp.2020_6034

Abstract

Background: Diabetic retinopathy (DR) is a diabetic complication with complex etiology and severe visual impairment. Dysregulated long noncoding RNAs (lncRNAs) are closely associated with DR. This article focused on the impact of lncRNA transmembrane phosphatase with tensin homology pseudogene 1 (TPTEP1) in DR. Methods: First, sera were collected from DR patients and healthy control. Human retinal vascular endothelial cells (HRVECs) were exposed to high glucose (HG) to construct a DR model in vitro. A real-time quantitative polymerase chain reaction (RT-qPCR) was carried out to detect TPTEP1. Targeting relationships were predicted using StarBase and TargetScan, and confirmed by the Dual-Luciferase Reporter Assay. Cell Counting Kit 8 (CCK-8) and EdU staining were applied to measure cell viability and proliferation, respectively. Protein expression was determined by a western blotting assay. Results: lncRNA TPTEP1 expression was significantly decreased in the serum of DR patients and HG-stimulated HRVECs. Overexpression of TPTEP1 reduced cell viability and proliferation induced by HG and oxidative stress. In addition, overexpression of miR-489-3p impaired the effects of TPTEP1. Nrf2, which was targeted by miR-489-3p, was down-regulated in HG-treatment HRVECs. Knockdown of Nrf2 enhanced the influence of miR-489-3p and antagonized the effects of TPTEP1. Conclusion: This study demonstrated that a TPTEP1/miR-489-3p/NRF2 axis affects the development of DR by regulating oxidative stress.

Published
2023-02-16
Issue
Vol. 70 No. 1 (2023)
Section
Articles

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