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Serum exosome microRNAs predict multiple sclerosis disease activity after fingolimod treatment

ABSTRACT: Serum exosome microRNAs predict multiple sclerosis disease activity after fingolimod treatment

PROVIDER: PRJNA588268 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10417200.fastq.gz	Fastqsanger.gz
	SRR10417300.fastq.gz	Fastqsanger.gz
	SRR10417201.fastq.gz	Fastqsanger.gz
	SRR10417301.fastq.gz	Fastqsanger.gz
	SRR10417202.fastq.gz	Fastqsanger.gz

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Serum exosome microRNAs predict multiple sclerosis disease activity after fingolimod treatment

Project description:Background: We and others have previously demonstrated the potential for circulating exosome microRNAs to aid in disease diagnosis. In this study, we sought the possible utility of serum exosome microRNAs as biomarkers for disease activity in multiple sclerosis patients in response to fingolimod therapy. We studied patients with relapsing-remitting multiple sclerosis prior to and 6 months after treatment with fingolimod. Methods: Disease activity was determined using gadolinium-enhanced magnetic resonance imaging. Serum exosome microRNAs were profiled using next-generation sequencing. Data were analysed using univariate/multivariate modelling and machine learning to determine microRNA signatures with predictive utility. Results: we identified 15 individual miRNAs that were differentially expressed in serum exosomes from post-treatment patients with active versus quiescent disease. The targets of these microRNAs clustered in ontologies related to the immune and nervous systems, and signal transduction. While the power of individual microRNAs to predict disease status post-fingolimod was modest (average 77%, range 65 to 91%), several combinations of 2 or 3 miRNAs were able to distinguish active from quiescent disease with greater than 90% accuracy. Further stratification of patients identified additional microRNAs associated with stable remission, and a positive response to fingolimod in patients with active disease prior to treatment. Conclusions: Overall, these data underscore the value of serum exosome microRNA signatures as non-invasive biomarkers of disease in multiple sclerosis and suggest they may be used to predict response to fingolimod in future clinical practice. Additionally, these data suggest that fingolimod may have mechanisms of action beyond its known functions.

2019-11-08 | GSE140106 | GEO

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Mouse serum exosome proteomics

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Project description:We developed TF-based MNPs (TF-MNPs) to isolate blood-derived exosome in this study and isolated the blood-derived exosomes of patients with neuroinflammatory diseases, such as dementia, Parkinson’s disease and multiple sclerosis via this strategy and then evaluated the proteomic profiling of these exosomes to screen for a potential candidate biomarker. Blood was collected from 10 patients in each of the three disease groups. Over 800 serum exosome proteins were identified by highly sensitive nanoflow liquid chromatography-tandem mass spectrometry (LC−MS/MS).

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Transcriptomic profile of multiple sclerosis patients treated with fingolimod

Project description:Fingolimod is an immunomodulatory sphingosine-1-phosphate (S1P) analogue approved for the treatment of relapsing-remitting multiple sclerosis (RRMS). The identification of biomarkers of clinical response to fingolimod is a major necessity in MS to identify optimal responders and avoid the risk of disease progression in non-responders. With this aim, we used RNA-sequencing to study the transcriptomic changes induced by fingolimod in peripheral blood mononuclear cells of MS-treated patients and their association with clinical response. Samples were obtained from 10 RRMS patients (5 responders and 5 non-responders) at baseline and at 12 months of fingolimod therapy. Fingolimod exerted a vast impact at the transcriptional level, identifying 7155 differentially expressed genes (DEGs) compared to baseline that affected the regulation of numerous signalling pathways and cellular processes. These DEGs were predominantly immune-related, including genes associated with S1P metabolism, cytokines, lymphocyte trafficking, master transcription factors of lymphocyte functions and the NF-kB pathway. Responder and non-responder patients exhibited a differential transcriptomic regulation during fingolimod treatment, with responders presenting a higher number of DEGs (6405) compared to non-responders (2653). These transcriptomic differences offer the potential of being exploited as biomarkers of clinical response to fingolimod.

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MicroRNA profile of exosome from serum samples of Kawasaki disease

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