ArticleAmerican journal of translational research2017
microRNA-383 mediates high glucose-induced oxidative stress and apoptosis in retinal pigment epithelial cells by repressing peroxiredoxin 3.
Article in American journal of translational research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- MicroRNAs: A Social Network in Diabetic Retinopathy.Biomolecules · 2026Review
- Precision Medicine in Diabetic Retinopathy: The Role of Genetic and Epigenetic Biomarkers.Journal of clinical medicine · 2025Review
- A miR-383-5p Signaling Hub Coordinates the Axon Regeneration Response to Inflammation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Mechanistic and therapeutic perspectives of non-coding RNA-modulated apoptotic signaling in diabetic retinopathy.Cell biology and toxicology · 2024Review
- Stem Cell-Derived Exosomes: Natural Intercellular Messengers with Versatile Mechanisms for the Treatment of Diabetic Retinopathy.International journal of nanomedicine · 2024Review
- A Concise Review of MicroRNA-383: Exploring the Insights of Its Function in Tumorigenesis.Journal of Cancer · 2022Review
- The Correlation Between MicroRNAs and Diabetic Retinopathy.Frontiers in immunology · 2022Review
- SIRT3 deficiency increases mitochondrial oxidative stress and promotes migration of retinal pigment epithelial cells.Experimental biology and medicine (Maywood, N.J.) · 2021Article
- Article
- The Role of MicroRNAs in Mitochondria-Mediated Eye Diseases.Frontiers in cell and developmental biology · 2021Review
- The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress.International journal of molecular sciences · 2020Review
- MicroRNA-140-5p ameliorates the high glucose-induced apoptosis and inflammation through suppressing TLR4/NF-κB signaling pathway in human renal tubular epithelial cells.Bioscience reports · 2020Article
- Analysis of miRNAs and their target genes associated with mucosal damage caused by transport stress in the mallard duck intestine.PloS one · 2020Article
- Effects of microRNA‑217 on high glucose‑induced inflammation and apoptosis of human retinal pigment epithelial cells (ARPE‑19) and its underlying mechanism.Molecular medicine reports · 2019Article
- NFE2/miR-423-5p/TFF1 axis regulates high glucose-induced apoptosis in retinal pigment epithelial cells.BMC molecular and cell biology · 2019Article
- Elevation of the vitreous body concentrations of oxidative stress-responsive apoptosis-inducing protein (ORAIP) in proliferative diabetic retinopathy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2019Article
- Down-regulation of microRNA-216a confers protection against yttrium aluminium garnet laser-induced retinal injuryJournal of biosciences · 2018Article
- Integrative machine learning analysis of multiple gene expression profiles in cervical cancer.PeerJ · 2018Article
- Control-released Alpha-lipoic acid-loaded PLGA microspheres enhance bone formation in type 2 diabetic rat model.International journal of clinical and experimental pathology · 2017Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperglycemia-mediated damage to retinal pigment epithelial (RPE) cells plays a central role in the pathogenesis of diabetic retinopathy. Dysregulation of microRNA (miR)-383 modulates pancreatic beta cell survival in diabetes; however, its role in diabetic retinopathy remains unclear. In this study, we examined the expression of miR-383 in ARPE-19 human RPE cell lines after high glucose treatment and investigated its functions in high glucose-induced reactive oxygen species (ROS) generation and apoptotic responses. The downstream target gene that mediated the action of miR-383 was functionally characterized. It was found that high glucose induced a 2.4-fold increase in miR-383 abundance, compared to ARPE-19 cells treated with normal glucose. Overexpression of miR-383 inhibited cell viability and promoted apoptosis and ROS formation in ARPE-19 cells, which was coupled with deregulation of Bcl-2 and Bax. Peroxiredoxin 3 (PRDX3) expression was repressed by miR-383 in ARPE-19 cells. Restoration of PRDX3 counteracted miR-383-induced ROS generation and apoptosis, while silencing of PRDX3 phenocopied the detrimental effects of miR-383 on ARPE-19 cells. Delivery of anti-miR-383 inhibitors led to an increase of PRDX3 expression and prevented high glucose-elicited ROS formation and apoptosis in ARPE-19 cells. Overall, miR-383 upregulation accounts for high glucose-induced oxidative stress and apoptosis in RPE cells by repressing PRDX3 expression. Targeting miR-383 may have therapeutic potential in the treatment of diabetic retinopathy.
Indexed as
Identifiers
28559987PMC5446519W3023087162What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.