ArticleClinical and experimental nephrology2022
KCNQ1OT1 inhibition alleviates high glucose-induced podocyte injury by adsorbing miR-23b-3p and regulating Sema3A.
Article in Clinical and experimental nephrology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Programmed Cell Death in Diabetic Kidney Disease: Mechanisms and Therapeutic Targeting.Journal of inflammation research · 2025Review
- The potential role of differentially expressed tRNA-derived fragments in high glucose-induced podocytes.Renal failure · 2024Article
- Long noncoding RNA protein-disulfide isomerase-associated 3 regulated high glucose-induced podocyte apoptosis in diabetic nephropathy through targeting miR-139-3p.World journal of diabetes · 2024Article
- Role of Semaphorin 3A in Kidney Development and Diseases.Diagnostics (Basel, Switzerland) · 2023Review
- Long Non-Coding RNAs in the Pathogenesis of Diabetic Kidney Disease.Frontiers in cell and developmental biology · 2022Review
- Natural antisense transcripts as drug targets.Frontiers in molecular biosciences · 2022Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundDiabetic nephropathy (DN), a diabetic complication, is the leading cause of end-stage renal disease. KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1), a long non-coding RNA, has been unmasked to participate in the pathogenesis of DN. However, the specific mechanism by which KCNQ1OT1 regulates podocyte injury remains unclear.
methodsRelative expression of KCNQ1OT1 was measured with quantitative real-time polymerase chain reaction (qRT-PCR). The levels of inflammatory cytokines were analyzed by enzyme linked immunosorbent assay (ELISA). The viability, proliferation, and apoptosis of high glucose (HG)-treated podocyte were analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), 5-ethynyl-2'-deoxyuridine (EdU), and flow cytometry assays. Protein levels were analyzed by western blotting. The regulatory mechanism of KCNQ1OT1 was surveyed by bioinformatics analysis, dual-luciferase reporter, and RNA immunoprecipitation (RIP) assays.
resultsWe observed an apparent upregulation in KCNQ1OT1 expression in serums of DN patients and HG-treated podocytes. Furthermore, KCNQ1OT1 downregulation alleviated HG-induced inflammation, proliferation repression, and apoptosis in podocytes. Notably, KCNQ1OT1 was identified as a miR-23b-3p sponge, and miR-23b-3p directly targeted Semaphorin-3A (Sema3A). Moreover, miR-23b-3p silencing reversed KCNQ1OT1 knockdown-mediated effects on inflammation, proliferation, and apoptosis of HG-induced podocytes. Also, Sema3A overexpression reversed the effects of miR-23b-3p mimic on inflammation, proliferation, and apoptosis of HG-induced podocytes. Importantly, KCNQ1OT1 regulated Sema3A expression by sponging miR-23b-3p.
conclusionsHG-induced KCNQ1OT1 promoted inflammation, proliferation repression, and apoptosis of podocytes via increasing Sema3A expression through sponging miR-23b-3p. This study provided evidence to support the involvement of KCNQ1OT1 in the pathogenesis of DN.
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