ArticleInternational urology and nephrology2022
LncRNA NEAT1 knockdown ameliorates LPS-induced human kidney injury by mediating the miR-330-5p/FOXO3 axis.
Article in International urology and nephrology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 6 citations in OpenAlex.
- Research progress on the mechanism of FOXO protein in sepsis.Apoptosis : an international journal on programmed cell death · 2026Review
- The NEAT1/miR-124-3p/CCL2 axis in chronic kidney disease progression: integrated bioinformatics analysis and experimental validation.Epigenomics · 2025Article
- Circulating Exosomes from Septic Mice Activate NF-κB/MIR17HG Pathway in Macrophages.Biomedicines · 2024Article
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4 authors at 2 institutions in 1 country.
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Abstract
backgroundSepsis is a systemic process with multiple inflammatory responses and organ injuries, particularly in the damage of the kidney. Recently, numerous studies suggest that long non-coding RNAs (lncRNAs) are involved in sepsis-related kidney injury. This study aimed to investigate the functional role and mechanism of lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) in sepsis-related kidney injury.
methodsCell model of kidney injury was constructed in human kidney 2 (HK-2) cells with the treatment of lipopolysaccharide (LPS). The expression of NEAT1 was measured by quantitative real-time PCR (qRT-PCR). Cell viability was examined using CCK-8 assay. Flow cytometry was performed to detect cell apoptosis, and apoptosis-related proteins were quantified by western blot. The release of proinflammatory cytokines was assessed by ELISA. Oxidative stress was assessed by the levels of SOD and MDA using kits. The putative relationship between miR-330-5p and NEAT1 or FOXO3 was confirmed using dual-luciferase reporter assay, RIP assay and pull-down assay.
resultThe expression of NEAT1 was increased in LPS-treated HK-2 cells. LPS exposure promoted apoptotic rate, inflammatory responses and oxidative stress in HK-2 cells, which were largely ameliorated by NEAT1 knockdown. MiR-330-5p was verified as a target of NEAT1, and miR-330-5p inhibition reversed the effects of NEAT1 knockdown in LPS-treated HK-2 cells. Moreover, FOXO3 was a target of miR-330-5p, and miR-330-5p restoration-blocked cell apoptosis, inflammation and oxidative stress in LPS-treated HK-2 cells were recovered by FOXO3 overexpression.
conclusionNEAT1 downregulation meliorated LPS-induced HK-2 cell injuries partly by regulating the miR-330-5p/FOXO3 pathway.
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