ArticleJournal of inflammation research2021
Inhibition of Long Non-Coding RNA KCNQ1OT1 Attenuates Neuroinflammation and Neuronal Apoptosis Through Regulating NLRP3 Expression via Sponging miR-30e-3p.
Article in Journal of inflammation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Long non-coding RNAs in glial cells: key drivers of neuroinflammation in cognitive disorders.Frontiers in aging neuroscience · 2026Pooled it
- DNA Topoisomerase IIβ Suppresses Microglial Inflammatory Cytokine Release: A Potential Regulator of Neuroinflammation.Neurochemical research · 2026Article
- HMC3 revealed: how much do these "Microglia" really tell us?Frontiers in immunology · 2026Review
- Extracellular Competing Endogenous RNA Networks Reveal Key Regulators of Early Amyloid Pathology Propagation in Alzheimer's Disease.International journal of molecular sciences · 2025Article
- Intestinal microenvironment dynamics and Sepsis-associated encephalopathy pathophysiology: insights from multi-omics profiling.Frontiers in neurology · 2025Article
- Emerging Role of Long Noncoding RNAs in Regulating Inflammasome-Mediated Neurodegeneration in Parkinson's Disease.Molecular neurobiology · 2024Review
- Selection of suitable reference genes for gene expression studies in HMC3 cell line by quantitative real-time RT-PCR.Scientific reports · 2024Article
- Ischemic Stroke and Autophagy: The Roles of Long Non-Coding RNAs.Current neuropharmacology · 2024Review
- Epigenetic modifications of DNA and RNA in Alzheimer's disease.Frontiers in molecular neuroscience · 2024Review
- Dysregulation of miRNA-30e-3p targeting IL-1β in an international cohort of systemic autoinflammatory disease patients.Journal of molecular medicine (Berlin, Germany) · 2023Article
- FAS-mediated circRNA-miRNA-mRNA Crosstalk Network Regulates Immune Cell Infiltration in Cerebral Infarction.Journal of molecular neuroscience : MN · 2023Article
- Long noncoding RNA Kcnq1ot1 prompts lipopolysaccharide-induced acute lung injury by microRNA-7a-5p/Rtn3 axis.European journal of medical research · 2022Article
- Clues for Improving the Pathophysiology Knowledge for Endometriosis Using Plasma Micro-RNA Expression.Diagnostics (Basel, Switzerland) · 2022Article
- KCNQ1OT1 Influences HK-2 Apoptosis and Inflammation in LPS-Induced Acute Renal Injury via Modulating miR-30a-5p/NLRP3 Axis.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Non-coding RNAs: The Neuroinflammatory Regulators in Neurodegenerative Diseases.Frontiers in neurology · 2022Review
- Potential of long non-coding RNA KCNQ1OT1 as a biomarker reflecting systemic inflammation, multiple organ dysfunction, and mortality risk in sepsis patients.Journal of clinical laboratory analysis · 2021Article
- Silencing Long Non-coding RNA Kcnq1ot1 Limits Acute Kidney Injury by Promoting miR-204-5p and Blocking the Activation of NLRP3 Inflammasome.Frontiers in physiology · 2021Article
- Long Non-Coding RNA-Mediated Competing Endogenous RNA Networks in Ischemic Stroke: Molecular Mechanisms, Therapeutic Implications, and Challenges.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeuroinflammation and neuronal apoptosis are considered as the critical factors in the pathogenesis of multiple neurological diseases. Recent studies have shown that long non-coding RNA (lncRNA) plays a crucial part in neuroinflammation and neuronal apoptosis.
methodsThe expression levels of lncRNA KCNQ1OT1, miR-30e-3p and NLRP3 in lipopolysaccharide (LPS)-induced HMC3 cells were analyzed using RT-qPCR. MTT assay, LDH release assay and ELISA were used to assess the effect of KCNQ1OT1 and miR-30e-3p on neuroinflammation and neuronal apoptosis. The targeted regulatory relationships among KCNQ1OT1, miR-30e-3p and NLRP3 were evaluated by bioinformatics analysis, dual-luciferase reporter gene assay, RT-qPCR and Western blot.
resultsIn LPS-induced HMC3 cells, the expression levels of KCNQ1OT1 and NLRP3 were increased, while the expression level of miR-30e-3p was reduced. Knockdown of KCNQ1OT1 alleviated LPS-induced apoptosis and neuroinflammation of HMC3 cells, accompanied by increased cell viability, low LDH release and reduced cell apoptosis rate, and reduced levels of TNF-α, IL-1β and IL-6. Overexpression of miR-30e-3p had a similar effect. Additionally, KCNQ1OT1 could bind with miR-30e-3p and repress its expression in HMC3 cells, and KCNQ1OT1 overexpression counteracted miR-30e-3p's inhibitory effect on LPS-induced neuronal damage and inflammatory response in HMC3 cells. Furthermore, KCNQ1OT1 could positively regulate the expression of NLRP3 via repressing miR-30e-3p.
conclusionInhibition of KCNQ1OT1 could reduce neuroinflammation and neuronal apoptosis induced by LPS in HMC3 cells by regulating miR-30e-3p/NLRP3 pathway, suggesting that KCNQ1OT1 and miR-30e-3p could serve as promising therapeutic targets for treating neurological diseases.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.