ArticleMolecular biology reports2016
Inhibition of the oxidative stress-induced miR-23a protects the human retinal pigment epithelium (RPE) cells from apoptosis through the upregulation of glutaminase and glutamine uptake.
Article in Molecular biology reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Complement C5a promotes human retinal pigment epithelial cell viability and migration through SLC38A1-mediated glutamine metabolism.Medical microbiology and immunology · 2025Article
- Differentially expressed microRNAs targeting genes in key pathways in keratoconus.Frontiers in genetics · 2024Article
- The Role of Retinal Dysfunction in Myopia Development.Cellular and molecular neurobiology · 2023Review
- Non-Coding RNAs Regulating Mitochondrial Functions and the Oxidative Stress Response as Putative Targets against Age-Related Macular Degeneration (AMD).International journal of molecular sciences · 2023Review
- Silencing of miR-23a attenuates hydrogen peroxide (HCytotechnology · 2020Article
- Oxidative stress-induced angiogenesis is mediated by miR-205-5p.Journal of cellular and molecular medicine · 2020Article
- The Impact of miRNAs in Health and Disease of Retinal Pigment Epithelium.Frontiers in cell and developmental biology · 2020Review
- miR302a and 122 are deregulated in small extracellular vesicles from ARPE-19 cells cultured with HScientific reports · 2019Article
- MicroRNAs play an important role in contributing to arsenic susceptibility in the chronically exposed individuals of West Bengal, India.Environmental science and pollution research international · 2019Article
- Literature-Based Enrichment Insights into Redox Control of Vascular Biology.Oxidative medicine and cellular longevity · 2019Review
- miRNAexpression profile of retinal pigment epithelial cells under oxidative stress conditions.FEBS open bio · 2018Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The degeneration of retinal pigment epithelium (RPE) cells in the sub retinal pigment epithelial space and choroid is an initial pathological characteristic for the age-related macular degeneration which is the leading cause of severe vision loss in old people. Moreover, oxidative stress is implicated as a major inducer of RPE cell death. Here, we assessed the correlation between the H2O2-induced RPE cell death and glutamine metabolism. We found under low glutamine supply (20 %), the ARPE-19 cells were more susceptive to H2O2-induced apoptosis. Moreover, the glutamine uptake and the glutaminase (GLS) were suppressed by H2O2 treatments. Moreover, we observed miR-23a was upregulated by H2O2 treatments and overexpression of miR-23a significantly sensitized ARPE-19 cells to H2O2. Importantly, Western blotting and luciferase assay demonstrated GLS1 is a direct target of miR-23a in RPE cells. Inhibition of the H2O2-induced miR-23a by antagomiR protected the RPE cells from the oxidative stress-induced cell death. In addition, recovery of GLS1 expression in miR-23a overexpressed RPE cells rescued the H2O2-induced cell death. This study illustrated a mechanism for the protection of the oxidative-induced RPE cell death through the recovery of glutamine metabolism by inhibition of miR-23a, contributing to the discovery of novel targets and the developments of therapeutic strategies for the prevention of RPE cells from oxidative stress.
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