ArticleChild's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery2021
miR-23a-3p is involved in drug resistance by directly targeting the influx drug transporter organic anion-transporting polypeptide 2.
Article in Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 6 citations in OpenAlex.
- Effect of high altitude on the pharmacokinetics and pharmacodynamics of valproate in epileptic rats.Frontiers in pharmacology · 2026Article
- Recent advances of miR-23 in human diseases and growth development.Non-coding RNA research · 2025Review
- Downregulation of miR-23a-3p improves cognitive function in rats after subarachnoid hemorrhage by targeting VCAN.Medical molecular morphology · 2022Article
- The molecular mechanism of circRHOBTB3 inhibits the proliferation and invasion of epithelial ovarian cancer by serving as the ceRNA of miR-23a-3p.Journal of ovarian research · 2022Article
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4 authors at 3 institutions in 1 country.
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Abstract
objectiveDrug transporters are involved in the drug resistance of individuals with drug-resistant epilepsy by influencing the intracerebral transport of antiepileptic drugs (AEDs). The expression of drug transporters is associated with microRNAs. We previously revealed that miR-23a-3p levels were elevated in the blood of patients with intractable epilepsy. Additionally, the influx drug transporter organic anion-transporting polypeptide 2 (Oatp2) is involved in the intracerebral transport of valproic acid (VPA), the most commonly used AED; repeated seizures lead to decreased expression of Oatp2. However, the role of miR-23a-3p in the expression of Oatp2 and in the development of drug resistance has not been established. Herein, we aimed to determine the potential role of miR-23a-3p in VPA-resistant epilepsy through in vivo and in vitro experiments.
methodsEpilepsy was elicited after status epilepticus (SE) was induced by lithium-pilocarpine in adult Sprague-Dawley rats, followed by VPA treatment to select rats with VPA resistance. The expression of miR-23a-3p was detected by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR). A miR-23a-3p inhibitor was intracerebrally injected into VPA-resistant rats, and histological staining and Morris water maze tests were performed to evaluate brain damage and learning/memory functions in these rats. Subsequently, a dual-luciferase reporter assay and a VPA uptake assay were performed in brain microvascular endothelial cells (BMECs) to investigate the underlying mechanism of action of miR-23a-3p.
resultsOur results indicated that compared to that in control rats, miR-23a-3p was elevated in VPA-resistant rats. Intracerebral injection of a miR-23a-3p inhibitor reduced brain damage and the associated deficits in learning and memory functions in rats with VPA resistance. Further investigation indicated that Oatp2 was the direct target of miR-23a-3p, and it was negatively regulated by miR-23a-3p in the brain and BMECs. Furthermore, we demonstrated that miR-23a-3p reduced VPA uptake in BMECs by regulating Oatp2 expression.
conclusionsmiR-23a-3p is involved in VPA resistance in epilepsy by directly targeting the influx drug transporter Oatp2, indicating that miR-23a-3p could be a potential therapeutic target for intractable epilepsy.
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