ArticleCell cycle (Georgetown, Tex.)2020
Overexpressed microRNA-494 represses RIPK1 to attenuate hippocampal neuron injury in epilepsy rats by inactivating the NF-κB signaling pathway.
Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- β-hydroxybutyrate regulates microglia M1/M2 polarization and phagocytosis through the JAK1/STAT1 pathway to reduce neuroinflammation and exert anti-epileptic effects.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Epigenetic Mechanisms in the Pathophysiology and Progression of Epilepsy: A Comprehensive Review of Experimental and Clinical Studies.Current neuropharmacology · 2025Review
- Involvement of extracellular vesicle microRNA clusters in developing healthy and Rett syndrome brain organoids.Cellular and molecular life sciences : CMLS · 2024Article
- Integrating Proteomics and Transcriptomics Reveals the Potential Pathways of Hippocampal Neuron Apoptosis in Dravet Syndrome Model Mice.International journal of molecular sciences · 2024Article
- PDCD4 silencing alleviates KA‑induced neurotoxicity of HT22 cells by inhibiting endoplasmic reticulum stress via blocking the MAPK/NF‑κB signaling pathway.Experimental and therapeutic medicine · 2024Article
- The dysregulation of miRNAs in epilepsy and their regulatory role in inflammation and apoptosis.Functional & integrative genomics · 2023Review
- Modulation of AKT Pathway-Targeting miRNAs for Cancer Cell Treatment with Natural Products.International journal of molecular sciences · 2023Review
- LncRNA ZFAS1 regulates the hippocampal neurons injury in epilepsy through the miR-15a-5p/OXSR1/NF-κB pathway.Metabolic brain disease · 2022Article
- Transcription factors are potential therapeutic targets in epilepsy.Journal of cellular and molecular medicine · 2022Review
- Aberrant expression of miRNAs in epilepsy.Molecular biology reports · 2022Review
- Mechanical ventilation induces lung and brain injury through ATP production, P2Y1 receptor activation and dopamine release.Bioengineered · 2022Review
- Linoleic Acid Upregulates Microrna-494 to Induce Quiescence in Colorectal Cancer.International journal of molecular sciences · 2021Article
- MicroRNA Dysregulation in Epilepsy: From Pathogenetic Involvement to Diagnostic Biomarker and Therapeutic Agent Development.Frontiers in molecular neuroscience · 2021Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe effects of microRNAs (miRNAs) have been identified in epilepsy (Ep) in recent years, our research was focused on the functions of miR-494 in Ep and its inner mechanisms.
methodsThe Ep modeled rats induced by lithium chloride-pilocarpine were treated with agomir-miR-494 or RIPK1-siRNA. The pathology of rat hippocampal tissues was observed. Expression of miR-494, receptor-interacting protein kinase 1 (RIPK1) and nuclear factor-kappaB (NF-κB) p65 was assessed by RT-qPCR and Western blot analysis. The hippocampal neurons of epileptic rats were successfully modeled, which were transfected with miR-494 mimics or RIPK1-siRNA to determine neurons' proliferation ability and cell apoptosis. The target relation between miR-494 and RIPK1 was measured by bioinformatics website and dual luciferase gene reporter assay.
resultsThe expression of miR-494 was reduced, while the expression of RIPK1 and NF-κB p65 was amplified in hippocampus of Ep rats. Elevated miR-494 repressed the expression of RIPK1 to ameliorate the hippocampal neuron injury, accelerate neuronal proliferation, and restrain neuronal apoptosis via inactivating the NF-κB signaling pathway, causing a deceleration of Ep development. Furthermore, amplified RIPK1 was able to reverse the amelioration of neuronal injury in Ep rats which was contributed by upregulated miR-494.
conclusionWe found in this study that elevated miR-494 repressed RIPK1, causing an inactivation of the NF-κB signaling pathway and acceleration of cell proliferation, and suppression of apoptosis of hippocampal neurons in Ep rats, thereby attenuating the neuron injury and Ep development. Our research may provide novel targets for the therapy of Ep.
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