ArticleApplied biochemistry and biotechnology2022
A Novel MIR503HG/miR-497-5p/CCL19 Axis Regulates High Glucose-Induced Cell Apoptosis, Inflammation, and Fibrosis in Human HK-2 Cells.
Article in Applied biochemistry and biotechnology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Co-host ncRNA MIR503HG/miR-503-5p antagonistically interfere with the crosstalk between fibroblasts and microvascular endothelial cells by affecting the production of LMW FGF2 in pterygium.International journal of ophthalmology · 2025Article
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- Tetramethylpyrazine promotes angiogenesis and nerve regeneration and nerve defect repair in rats with spinal cord injury.Heliyon · 2023Article
- The dysregulation of plasma miR-497/FGF23 axis, and its association with clinical characteristics and major adverse cardiovascular event in female premature acute coronary syndrome patients.Irish journal of medical science · 2023Article
- Microarray Expression Profile of Exosomal circRNAs from High Glucose Stimulated Human Renal Tubular Epithelial Cells.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Article
- Circular RNA MELK Promotes Chondrocyte Apoptosis and Inhibits Autophagy in Osteoarthritis by Regulating MYD88/NF-Contrast media & molecular imaging · 2022Article
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3 authors.
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Abstract
Long non-coding RNAs (lncRNAs) play crucial roles in the development of diabetic nephropathy (DN). Here, we explored the activity and mechanism of MIR503 host gene (MIR503HG) in high glucose (HG)-evoked cytotoxicity in HK-2 cells. MIR503HG, microRNA (miR)-497-5p, and C-C motif chemokine ligand 19 (CCL19) were quantified by quantitative real-time PCR (qRT-PCR) and western blot. The direct relationship between miR-497-5p and MIR503HG or CCL19 was confirmed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Cell viability and apoptosis were evaluated by XTT assay and flow cytometry, respectively. Our data showed that MIR503HG was overexpressed in HG-stimulated HK-2 cells. Knockdown of MIR503HG alleviated HG-evoked cell apoptosis, inflammation, and fibrosis in HK-2 cells. Mechanistically, MIR503HG regulated miR-497-5p expression via a binding site. MIR503HG depletion reduced HG-evoked cell apoptosis, inflammation, and fibrosis in HK-2 cells by up-regulating miR-497-5p. Moreover, miR-497-5p directly targeted and suppressed CCL19. MiR-497-5p-mediated suppression of CCL19 relieved HG-induced cell apoptosis, inflammation, and fibrosis in HK-2 cells. Furthermore, MIR503HG regulated CCL19 expression via miR-497-5p competition. Our findings identify a new MIR503HG/miR-497-5p/CCL19 network in the regulating HG-evoked cell apoptosis, inflammation, and fibrosis in HK-2 cells.
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