ArticleAging2021
miR-485 inhibits histone deacetylase HDAC5, HIF1α and PFKFB3 expression to alleviate epilepsy in cellular and rodent models.
Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- TRPV4 is involved in NLRP3 and NLRP1 inflammasomes activation after pilocarpine-induced status epilepticus in mice : Concise title: TRPV4-mediated inflammasome activation in epilepsy.Cellular and molecular life sciences : CMLS · 2026Article
- The dysregulation and regulatory mechanism of long non-coding RNA LBX2-AS1 in children with epilepsy.Italian journal of pediatrics · 2025Article
- SRF Facilitates Transcriptional Inhibition of Gem Expression by m6A Methyltransferase METTL3 to Suppress Neuronal Damage in Epilepsy.Molecular neurobiology · 2025Article
- The Role of Histone Deacetylases in NLRP3 Inflammasomesmediated Epilepsy.Current molecular medicine · 2024Review
- The lactate metabolism and protein lactylation in epilepsy.Frontiers in cellular neuroscience · 2024Review
- EGR1-Driven METTL3 Activation Curtails VIM-Mediated Neuron Injury in Epilepsy.Neurochemical research · 2023Article
- Altered miRNA Expression Profiles in the Serum of Beagle Dogs Experimentally Infected withAnimals : an open access journal from MDPI · 2023Article
- Stage- and Subfield-Associated Hippocampal miRNA Expression Patterns after Pilocarpine-Induced Status Epilepticus.Biomedicines · 2022Article
- miR-3960 from Mesenchymal Stem Cell-Derived Extracellular Vesicles Inactivates SDC1/Wnt/Stem cells international · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated the role of microRNA (miR)-485 and its downstream signaling molecules on mediating epilepsy in cellular and rat models. We established a cellular epilepsy model by exposing hippocampal neurons to magnesium and a rat model by treating ICR mice with lithium chloride (127 mg/kg) and pilocarpine (30 mg/kg). We confirmed that miR-485 could bind and inhibit histone deacetylase 5 (HDAC5) and then measured expression of miR-485 and in mice and cells. Cells were transfected with overexpression or knockdown of miR-485, HDAC5, hypoxia-inducible factor-1alpha (HIF1α), or 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 enzyme (PFKFB3) to verify their roles in apoptosis, oxidative stress, and inflammation in epileptic hippocampal neurons. Binding relationship between miR-485, HDAC5, HIF1α, and PFKFB3 was verified. Oxidative stress and inflammation marker levels in epilepsy model mice were assessed. miR-485 was downregulated and HDAC5 was upregulated in cell and animal model of epilepsy. Seizure, neuronal apoptosis, oxidative stress (increased SOD and GSH-Px expression and decreased MDA and 8-OHdG expression) and inflammation (reduced IL-1β, TNF-α, and IL-6 expression) were reduced by miR-485 in epileptic cells. HIF1α and PFKFB3 expression was reduced by HDAC5 knockdown in cells, which was recapitulated
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