Differential expression of miR-34a, 451, 1260, 1275 and 1298 in the neocortex of patients with mesial temporal lobe epilepsy

Organista‐Juárez, Diana; Jiménez, Adriana; Rocha, Luísa; Alonso-Vanegas, Mario; Guevara‐Guzmán, Rosalinda

doi:10.1016/j.eplepsyres.2019.106188

Cited by 18 publications

(18 citation statements)

References 40 publications

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“…28 Furthermore, hsa-miR-1275 has been identified to be differentially expressed in mesial temporal lobe epilepsy (mTLE) with hippocampal sclerosis (HS). 29,30 However, the knowledge about the regulation of miR-1275 in epilepsy is limited. In this study, hsa-miR-1275 was chosen based on DAVID analysis for target genes, which reveals that hsa-miR-1275 is involved in the regulation of obsolete synapse part, postsynaptic density, and postsynaptic membrane.…”

Section: Discussionmentioning

confidence: 99%

Identification of hsa-miR-1275 as a Novel Biomarker Targeting MECP2 for Human Epilepsy of Unknown Etiology

Zhao

Wang

et al. 2020

Molecular Therapy - Methods & Clinical Development

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Epilepsy affects around 70 million people worldwide, with a 65% rate of unknown etiology. This rate is known as epilepsy of unknown etiology (EUE). Dysregulation of microRNAs (miRNAs) is recognized to contribute to mental disorders, including epilepsy. However, miRNA dysregulation is poorly understood in EUE. Here, we conducted miRNA expression profiling of EUE by microarray technology and identified 57 pathogenic changed miRNAs with significance. The data and bioinformatic analysis results indicated that among these miR-NAs, hsa-microRNA (miR)-1275 was highly associated with neurological disorders. Subsequently, new samples of serum and cerebrospinal fluid were collected for validation of hsa-miR-1275 expression by TaqMan assays. Results show that hsa-miR-1275 in serums of EUE were increased significantly, but in cerebrospinal fluid, the miRNA was decreased. Moreover, the MECP2 gene was selected as a hsa-miR-1275 target based on target prediction tools and gene ontology analysis. Validation of in vitro tests proved that MECP2 expression was specifically inhibited by hsa-miR-1275. Additionally, overexpression of hsa-miR-1275 can elevate expression of nuclear factor kB (NF-kB) and promote cell apoptosis. Taken together, hsa-miR-1275 might represent a novel biomarker targeting MECP2 for human EUE.

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Section: Discussionmentioning

confidence: 99%

Identification of hsa-miR-1275 as a Novel Biomarker Targeting MECP2 for Human Epilepsy of Unknown Etiology

Zhao

Wang

et al. 2020

Molecular Therapy - Methods & Clinical Development

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“…23 Aberrant protein production with prominent transcriptional suppression creates a backdrop for these processes. 24,25 Key Points • A literature review was conducted on the biomarker potential of miRNAs in the early assessment of therapy response • A brief discussion of miRNA biology and the role of miRNAs in epilepsy and pharmacoresistance is provided • The most significant results in tissue and serum profiling and studies on animal models and cell cultures are discussed in more detail • Independently validated miRNAs are highlighted • An overview of general study design pitfalls and suggestions for future research are provided MicroRNAs (miRNAs) are a class of short noncoding RNAs (21-25 nucleotides long) functioning as important negative posttranscriptional regulators of gene expression. 26,27 There are approximately 2300 distinct miRNAs in the human genome estimated, 28 of which about 600 are well studied, and many are strongly conserved among species.…”

Section: Biomarker Potential In Epilepsymentioning

confidence: 99%

MicroRNAs in the development of resistance to antiseizure drugs and their potential as biomarkers in pharmacoresistant epilepsy

et al. 2021

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Epilepsy is a group of heterogeneous syndromes affecting more than 50 million people worldwide. Although many new antiseizure drugs (ASDs) have been developed in the past decade, approximately 30%-40% of patients remain pharmacoresistant (drug-resistant epilepsy [DRE], pharmacoresistant epilepsy, intractable epilepsy, refractory epilepsy). Furthermore, up to now, no effective treatment exists to prevent the development of epilepsy despite

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“…In addition to traditional targets such as ion channels, neurotransmitter receptors, and neurotransmitter transporters, important targets include mTOR and related pathways, the extracellular matrix, oxidative stress, anti-inflammatory pathways, neurosteroid systems, micro-RNAs, and epigenetic targets include histone deacetylase. 30,31,[63][64][65][66][67] Cell replacement strategies to introduce engineered cells that can support or release neuroactive substances and oligonucleotide approaches to regulate specific genes for therapeutic gain are also opportunities to identify new ways to treat refractory epilepsy. Moreover, clarification of the mechanisms underlying the ketogenic diet might identify metabolic and lipid targets that are relevant, the role of the gut microbiota, 68 and allow a "ketogenic diet in a pill" treatment strategy for refractory epilepsy.…”

Section: Refractory Epilepsymentioning

confidence: 99%

Epilepsy Benchmarks Area III: Improved Treatment Options for Controlling Seizures and Epilepsy-Related Conditions Without Side Effects

et al. 2020

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The goals of Epilepsy Benchmark Area III involve identifying areas that are ripe for progress in terms of controlling seizures and patient symptoms in light of the most recent advances in both basic and clinical research. These goals were developed with an emphasis on potential new therapeutic strategies that will reduce seizure burden and improve quality of life for patients with epilepsy. In particular, we continue to support the proposition that a better understanding of how seizures are initiated, propagated, and terminated in different forms of epilepsy is central to enabling new approaches to treatment, including pharmacological as well as surgical and device-oriented approaches. The stubbornly high rate of treatment-resistant epilepsy—one-third of patients—emphasizes the urgent need for new therapeutic strategies, including pharmacological, procedural, device linked, and genetic. The development of new approaches can be advanced by better animal models of seizure initiation that represent salient features of human epilepsy, as well as humanized models such as induced pluripotent stem cells and organoids. The rapid advances in genetic understanding of a subset of epilepsies provide a path to new and direct patient-relevant cellular and animal models, which could catalyze conceptualization of new treatments that may be broadly applicable across multiple forms of epilepsies beyond those arising from variation in a single gene. Remarkable advances in machine learning algorithms and miniaturization of devices and increases in computational power together provide an enhanced opportunity to detect and mitigate seizures in real time via devices that interrupt electrical activity directly or administer effective pharmaceuticals. Each of these potential areas for advance will be discussed in turn.

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Differential expression of miR-34a, 451, 1260, 1275 and 1298 in the neocortex of patients with mesial temporal lobe epilepsy

Cited by 18 publications

References 40 publications

Identification of hsa-miR-1275 as a Novel Biomarker Targeting MECP2 for Human Epilepsy of Unknown Etiology

Identification of hsa-miR-1275 as a Novel Biomarker Targeting MECP2 for Human Epilepsy of Unknown Etiology

MicroRNAs in the development of resistance to antiseizure drugs and their potential as biomarkers in pharmacoresistant epilepsy

Epilepsy Benchmarks Area III: Improved Treatment Options for Controlling Seizures and Epilepsy-Related Conditions Without Side Effects

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