ArticleJournal of endocrinological investigation2023
Hsa_circ_0003928 regulates the progression of diabetic nephropathy through miR-136-5p/PAQR3 axis.
Article in Journal of endocrinological investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Circ_0039857: A Key Player in Combating Immune Disorders and Ferroptosis in High-Glucose-induced HK-2 Cells and Diabetic Kidney Disease Mice.Applied biochemistry and biotechnology · 2026Article
- Circular RNAs in diabetes mellitus and its complications: a systematic review and in silico analyses.Endocrine connections · 2025Article
- Expression of urinary exosomal miR-136-5p in diabetic kidney disease and evaluation of its clinical diagnostic value.Scientific reports · 2025Article
- Programmed Cell Death in Diabetic Kidney Disease: Mechanisms and Therapeutic Targeting.Journal of inflammation research · 2025Review
- Molecular Mechanisms and Roles of MiR-136-5p in Human Cancer and Other Disorders.Current medicinal chemistry · 2025Review
- METTL14 derived from exosomes of M1 macrophages promotes high glucose-induced apoptosis, inflammation and oxidative stress in glomerular endothelial cells by mediating PAQR3 m6A modification.Clinical and experimental nephrology · 2024Article
- Hsa_circ_0008360 promotes high glucose-induced damage in HK-2 cells via miR-346/WNT2B axis.Journal of endocrinological investigation · 2024Article
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6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiabetic nephropathy (DN) is one of the complications of diabetes and has a high mortality, but its specific pathogenesis is not clear. In recent years, researches on the mechanism of circRNAs in DN have been proved a lot, whereas the functional mechanism of circ_0003928 in DN remains open and it must be investigated to value its important role in DN prevention.
methodsHK-2 cells were treated with high glucose (HG), normal glucose (NG) or Mannitol. Cell counting kit-8 (CCK8) and 5-ethynyl-2'-deoxyuridine (EdU) assays were performed to detect cell proliferation. Enzyme-linked immunosorbent assay (ELISA) was applied to analyze malondialdehyde (MDA) and superoxide dismutase 1 (SOD) levels. Flow cytometry and western blot were preformed to measure cell apoptosis. Real-time quantitative PCR (RT-qPCR) was used to test the levels of circ_0003928, miR-136-5p and progestin and adipoQ receptor family member 3 (PAQR3) mRNA. Western blot was executed to detect Bcl2 associated X (Bax), B cell leukemia/lymphoma 2 (Bcl2), smooth muscle (αSMA), apolipoprotein (C-IV) and PAQR3 levels. Luciferase reporter assay and RNA pull-down assay were used to analyze the target relationship between miR-136-5p and circ_0003928 or PAQR3.
resultsCirc_0003928 and PAQR3 expression were up-regulated, whereas miR-136-5p was decreased in DN serum and HG-induced HK-2 cells. Circ_0003928 knockdown promoted cell proliferation, and inhibit cell apoptosis, oxidative stress, and fibrosis in HK-2 cells under HG condition. MiR-136-5p silencing overturned the protective effects of si-circ_0003928 on HG-induced HK-2 cells. MiR-136-5p was targeted by circ_0003928 and directly targeted PAQR3. Overexpression of PAQR3 counteracted the inhibitory functions of circ_0003928 knockdown or miR-136-5p overexpression on HG-induced HK-2 cell injury.
conclusionCirc_0003928 acted as a sponge of miR-136-5p to up-regulating PAQR3 expression, and then regulate the proliferation, oxidative stress, fibrosis and apoptosis in HG-induced HK-2 cells.
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