Pathophysiology and Clinical Utility of Non-coding RNAs in Epilepsy

Shao, Yiye; Chen, Yinghui

doi:10.3389/fnmol.2017.00249

Cited by 33 publications

(27 citation statements)

References 105 publications

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“…Looking for “circulating diagnostic miRNA in human epilepsy,” we found only 6 papers in PubMed (November 2017). To identify a reliable diagnostic biomarker able to identify the pathology, we analyzed those 6 publications 87 , 88 , 89 , 90 , 91 , 92 and the results are presented here ( Table 3 ).…”

Section: Main Textmentioning

confidence: 99%

“…In the sixth paper, 92 a comparative analysis of circulating miRNAs in epilepsy has been proposed. In recent years, several miRNAs have been proposed as circulating biomarkers, showing dynamic changes of miRNA expression in relation to the history of the pathology.…”

Section: Main Textmentioning

confidence: 99%

“…Some miRNAs could be expressed soon after the onset of seizures (i.e., miR-9a-3p), whereas others were expressed only after the chronicization of the disease (i.e., miR-21-5p). 92 …”

Section: Main Textmentioning

confidence: 99%

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Potential Role of miRNAs as Theranostic Biomarkers of Epilepsy

Cava

Manna

Gambardella

et al. 2018

Molecular Therapy - Nucleic Acids

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Epilepsy includes a group of disorders of the brain characterized by an enduring predisposition to generate epileptic seizures. Although familial epilepsy has a genetic component and heritability, the etiology of the majority of non-familial epilepsies has no known associated genetic mutations. In epilepsy, recent epigenetic profiles have highlighted a possible role of microRNAs in its pathophysiology. In particular, molecular profiling identifies a significant number of microRNAs (miRNAs) altered in epileptic hippocampus of both animal models and human tissues. In this review, analyzing molecular profiles of different animal models of epilepsy, we identified a group of 20 miRNAs commonly altered in different epilepsy-animal models. As emerging evidences highlighted the poor overlap between signatures of animal model tissues and human samples, we focused our analysis on miRNAs, circulating in human biofluids, with a principal role in epilepsy hallmarks, and we identified a group of 8 diagnostic circulating miRNAs. We discussed the functional role of these 8 miRNAs in the epilepsy hallmarks. A few of them have also been proposed as therapeutic molecules for epilepsy treatment, revealing a great potential for miRNAs as theranostic molecules in epilepsy.

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Section: Main Textmentioning

confidence: 99%

Section: Main Textmentioning

confidence: 99%

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Potential Role of miRNAs as Theranostic Biomarkers of Epilepsy

Cava

Manna

Gambardella

et al. 2018

Molecular Therapy - Nucleic Acids

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“…Multiple studies have reported that miRNA levels in the circulating system were altered in correlation with certain pathological conditions, suggesting that circulating miRNA might become biomarkers for such diseases, including epilepsy [32, 46-49]. For example, in one genome-wide circulating miRNA expression profiling study, miR-106b-5p was found to have the best diagnostic value for epilepsy [50].…”

Section: Discussionmentioning

confidence: 99%

Silencing MicroRNA-155 Attenuates Kainic Acid-Induced Seizure by Inhibiting Microglia Activation

Huang

Cheng

Luo

et al. 2019

Neuroimmunomodulation

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Objective(s): Neuroinflammation is an important contributor to the development of seizures and epilepsy. Micro-RNA-155 (miR-155) plays a critical role in immunity and inflammation. This study aims to explore the function of miR-155 and miR-155-mediated inflammation in epilepsy. Methods: About 8-week-old male C57BL/6 mice were administered an intraperitoneal injection (i.p.) of kainic acid (KA) (15 mg/kg) or saline. The mice in the KA group developing acute seizure were further subjected to intracerebroventricular injection (i.c.v.) of antagomir negative control (NC) or miR-155 antagomir. Animal behavior was observed according to Racine’s scale, and electroencephalographs were recorded. Primary microglia were cultured and treated with antagomir NC or antagomir. Whole-cell electrophysiological recording was conducted to detect the spontaneous EPSCs and IPSCs in the neurons treated with different conditioned medium from those microglia. miR-155 were detected by qRT-PCR in those models, as well as in the brain or blood from epileptic patients and healthy controls. Results: miR-155 was abundantly expressed in glial cells compared with neurons, and its expression was markedly elevated in the brain of epilepsy patients and KA-induced seizure mice. Silencing miR-155 attenuated KA-induced seizure, abnormal electroencephalography, proinflammatory cytokine expression, and microglia morphology change. Moreover, conditioned media from KA-treated microglia impaired neuron excitability, whereas conditioned media from KA and miR-155 antagomir co-treated microglia had no such effects. Finally, miR-155 levels were significantly higher in the blood of epilepsy patients than those of healthy controls. Conclusion(s): These findings demonstrate that aberrant upregulation of miR-155 contributes to epileptogenesis through inducing microglia neuroinflammation.

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“…Nowadays, it is also debated that miRNAs can have a nuclear function by modulating gene expression directly at the transcriptional level (reviewed by Catalanotto et al, 2016). Numerous miRNAs have been identified in relation to epilepsy pathogenesis (reviewed by Reschke and Henshall, 2015;Henshall et al, 2016;Shao and Chen, 2017;Tiwari et al, 2018), and also several ion channels appear to be under control of miRNAs, including K v 1.1, K v 4.2, Kcnk10 and Grin2a (Sosanya et al, 2013;Alsharafi et al, 2016;Gross et al, 2016;Haenisch et al, 2016;Tiwari et al, 2019; Table 1).…”

Section: Regulation Of Acquired Ion Channelopathies By Micrornasmentioning

confidence: 99%

Transcriptional Regulation of Channelopathies in Genetic and Acquired Epilepsies

Loo

Becker

2020

Front. Cell. Neurosci.

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Epilepsy is a common neurological disorder characterized by recurrent uncontrolled seizures and has an idiopathic "genetic" etiology or a symptomatic "acquired" component. Genetic studies have revealed that many epilepsy susceptibility genes encode ion channels, including voltage-gated sodium, potassium and calcium channels. The high prevalence of ion channels in epilepsy pathogenesis led to the causative concept of "ion channelopathies," which can be elicited by specific mutations in the coding or promoter regions of genes in genetic epilepsies. Intriguingly, expression changes of the same ion channel genes by augmentation of specific transcription factors (TFs) early after an insult can underlie acquired epilepsies. In this study, we review how the transcriptional regulation of ion channels in both genetic and acquired epilepsies can be controlled, and compare these epilepsy "ion channelopathies" with other neurodevelopmental disorders.

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Pathophysiology and Clinical Utility of Non-coding RNAs in Epilepsy

Cited by 33 publications

References 105 publications

Potential Role of miRNAs as Theranostic Biomarkers of Epilepsy

Potential Role of miRNAs as Theranostic Biomarkers of Epilepsy

Silencing MicroRNA-155 Attenuates Kainic Acid-Induced Seizure by Inhibiting Microglia Activation

Transcriptional Regulation of Channelopathies in Genetic and Acquired Epilepsies

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