ArticleInternational ophthalmology2020
Long non-coding RNA Arid2-IR affects advanced glycation end products-induced human retinal endothelial cell injury by binding to Smad3.
Article in International ophthalmology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Oxidative Stress and Its Regulation in Diabetic Retinopathy.Antioxidants (Basel, Switzerland) · 2023Review
- Review
- Diabetic Retinopathy: Are lncRNAs New Molecular Players and Targets?Antioxidants (Basel, Switzerland) · 2022Review
- SIS3 Alleviates Cisplatin-Induced Acute Kidney Injury by Regulating the LncRNA Arid2-IR-Transferrin Receptor Pathway.Kidney & blood pressure research · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeLong non-coding RNAs (lncRNAs) have been reported to play significant roles in the pathogenesis of diabetic retinopathy (DR). The aim of the present study was to investigate the role of lncRNA Arid2-IR in advanced glycation end product (AGE)-induced human retinal endothelial cells (HRECs) injury. MATERIALS AND
methodsCell viability was determined by Cell Counting Kit-8 assay following induction with AGEs. The expression of Arid2-IR and Smad3 was detected by reverse transcription-quantitative PCR or western blotting. A luciferase reporter assay was conducted to determine the interaction between Arid2-IR and Smad3. The levels of inflammation-related and oxidative stress-related factors were evaluated by respective kits. The expression of extracellular matrix (ECM)-related and apoptosis-related proteins was detected by western blotting. Immunofluorescence assay was used to detect the level of vascular endothelial growth factor, and flow cytometry was applied to measure the levels of apoptosis.
resultsThe results revealed that AGE treatment decreased HREC proliferation and upregulated the expression of Arid2-IR and Smad3. The luciferase assay indicated that Smad3 was able to bind to the promoter region sequence of Arid2-IR. Moreover, Arid2-IR silencing reduced inflammation, oxidative stress and ECM production induced by AGEs in HRECs, and Smad3 inhibition further reduced the levels of the aforementioned factors, while Smad3 overexpression exerted the opposite effect. Furthermore, apoptosis of HRECs induced by AGEs was decreased following Arid2-IR silencing, which was further reduced following treatment with Smad3 inhibitor, but was reversed after transfection with Smad3 pcDNA3.1.
conclusionThe findings demonstrated that Arid2-IR affects AGE-induced HREC injury by binding to Smad3.
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