A miRNA signature in leukocytes from sporadic amyotrophic lateral sclerosis

Felice, Bruna De; Guida, Marco; Guida, Maurizio; Coppola, Cinzia; Mieri, Giovanna De; Cotrufo, Roberto

doi:10.1016/j.gene.2012.07.058

Cited by 126 publications

(124 citation statements)

References 37 publications

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“…Of particular interest, miRNA dysregulation is linked to aging and neurodegenerative disorders, including PD, AD, and multiple sclerosis (Goodall et al, 2013; Li et al, 2011; Ma et al, 2014). miRNA alterations are also present in microglial and neuronal cells in rodent ALS models and in peripheral blood mononuclear cells (PBMCs), fibroblasts, cerebrospinal fluid, and postmortem tissue from ALS subjects (Butovsky et al, 2012; Campos-Melo et al, 2013; De Felice et al, 2012; Freischmidt et al, 2014; Koval et al, 2013a; Kye and Goncalves Ido, 2014; Shinde et al, 2013), results which all support our observed DEmiRNAs in postmortem ALS spinal cord tissue. DEmiRNAs are likewise present in serum from pre-manifest fALS mutation carriers, suggesting both a role for miRNAs in ALS pathogenesis and as potential diagnostic biomarkers (Freischmidt et al, 2014).…”

Section: Discussionsupporting

confidence: 85%

Expression of microRNAs in human post-mortem amyotrophic lateral sclerosis spinal cords provides insight into disease mechanisms

Figueroa‐Romero

Hur

Lunn

et al. 2016

Molecular and Cellular Neuroscience

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Amyotrophic lateral sclerosis is a late-onset and terminal neurodegenerative disease. The majority of cases are sporadic with unknown causes and only a small number of cases are genetically linked. Recent evidence suggests that post-transcriptional regulation and epigenetic mechanisms, such as microRNAs, underlie the onset and progression of neurodegenerative disorders; therefore, altered microRNA expression may result in the dysregulation of key genes and biological pathways that contribute to the development of sporadic amyotrophic lateral sclerosis. Using systems biology analyses on postmortem human spinal cord tissue, we identified dysregulated mature microRNAs and their potential targets previously implicated in functional process and pathways associated with the pathogenesis of ALS. Furthermore, we report a global reduction of mature microRNAs, alterations in microRNA processing, and support for a role of the nucleotide binding protein, TAR DNA binding protein 43, in regulating sporadic amyotrophic lateral sclerosis-associated microRNAs, thereby offering a potential underlying mechanism for sporadic amyotrophic lateral sclerosis.

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Section: Discussionsupporting

confidence: 85%

Expression of microRNAs in human post-mortem amyotrophic lateral sclerosis spinal cords provides insight into disease mechanisms

Figueroa‐Romero

Hur

Lunn

et al. 2016

Molecular and Cellular Neuroscience

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“…Small non-coding RNAs (sncRNAs) are essential post-transcriptional gene regulation elements that are critical to immune system and neurodegenerative diseases [3-5] by affecting mRNA stability and the expression of multiple genes. Therefore, it is becoming increasingly evident that sncRNA species, as microRNAs, are associated with the development and progression of MS disease [6,7].…”

Section: Introductionmentioning

confidence: 99%

Small non-coding RNA signature in multiple sclerosis patients after treatment with interferon-β

et al. 2014

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BackgroundNon-coding small RNA molecules play pivotal roles in cellular and developmental processes by regulating gene expression at the post-transcriptional level. In human diseases, the roles of the non-coding small RNAs in specific degradation or translational suppression of the targeted mRNAs suggest a potential therapeutic approach of post-transcriptional gene silencing that targets the underlying disease etiology. The involvement of non-coding small RNAs in the pathogenesis of neurodegenerative diseases such as Alzheimer’s , Parkinson’s disease and Multiple Sclerosis has been demonstrated. Multiple sclerosis (MS) is an autoimmune disease of the central nervous system, characterized by chronic inflammation, demyelination and scarring as well as a broad spectrum of signs and symptoms. The current standard treatment for SM is interferon ß (IFNß) that is less than ideal due to side effects. In this study we administered the standard IFN-ß treatment to Relapsing-Remitting MS patients, all responder to the therapy; then examined their sncRNA expression profiles in order to identify the ncRNAs that were associated with MS patients’ response to IFNß.Methods40 IFNß treated Relapsing-Remitting MS patients were enrolled. We analyzed the composition of the entire small transcriptome by a small RNA cloning method, using peripheral blood from Relapsing-Remitting MS patients at baseline and 3 and 6 months after the start of IFNß therapy. Real-time qPCR from the same patients group and from 20 additional patients was performed to profile miRNAs expression.ResultsBeside the altered expression of several miRNAs, our analyses revealed the differential expression of small nucleolar RNAs and misc-RNAs.For the first time, we found that the expression level of miR-26a-5p changed related to INF-β response. MiR-26a-5p expression was significantly higher in IFN-β treated RRMS patients at 3 months treatment, keeping quite stable at 6 months treatments.ConclusionsOur results might provide insights into the mechanisms of action of IFN-β treatment in MS and provide fundamentals for the development of new biomarkers and/or therapeutic tools.

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“…Glutamate clearance is necessary for proper synaptic activation and to prevent neuronal damage from excessive activation of glutamate receptors (http://www.ncbi.nlm.nih.gov/gene?term = scl1a2). Dysfunction of EAAT2 and accumulation of excessive extracellular glutamate have been related to the development of several neurodegenerative diseases including Alzheimer's disease, Huntington's disease, and amyotrophic lateral sclerosis [8,9].…”

Section: Introductionmentioning

confidence: 99%

No association of the SLC1A2 rs3794087 allele with risk for essential tremor in the Spanish population

García‐Martín¹,

Martı́nez

Alonso‐Navarro

et al. 2013

Pharmacogenetics and Genomics

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A miRNA signature in leukocytes from sporadic amyotrophic lateral sclerosis

Cited by 126 publications

References 37 publications

Expression of microRNAs in human post-mortem amyotrophic lateral sclerosis spinal cords provides insight into disease mechanisms

Expression of microRNAs in human post-mortem amyotrophic lateral sclerosis spinal cords provides insight into disease mechanisms

Small non-coding RNA signature in multiple sclerosis patients after treatment with interferon-β

No association of the SLC1A2 rs3794087 allele with risk for essential tremor in the Spanish population

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