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ExpertMIX stratification of molecular profiles and clinical disease severity of RRMS patients

ABSTRACT: Whole blood expression was profiled in Relapsing Remitting Multiple Sclerosis patients

ORGANISM(S): Homo sapiens

PROVIDER: GSE61240 | GEO | 2017/09/10

SECONDARY ACCESSION(S): PRJNA260590

REPOSITORIES: GEO

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Disease modifying therapy impacts on miRNA expression profiling in peripheral blood from Relapsing-Remitting Multiple Sclerosis patients

Project description:Multiple sclerosis (MS) is a chronic and progressive neurological disease. MS is characterized by early-stage neuroinflammation, neurodegeneration, and demyelination, with a spectrum of heterogeneous clinical manifestations in terms of disease course and response to therapy. The currently unsatisfied availability of diagnostic and prognostic biomarkers concerning disease progression and treatment response represents an important requirement for therapy individualization and drug efficacy. Specific Disease Therapies (DMTs) are available to prevent MS-related brain damage; however, the specific drug choice is still under debate and needs further characterization. Since differentially expressed miRNAs have been proposed as diagnostic tools in neurodegenerative/neuro-inflammatory diseases, such as multiple sclerosis, amyotrophic lateral sclerosis, and Alzheimer's disease, we characterized the miRNA expression profiling in peripheral blood mononuclear cells (PBMC) of subjects with relapsing-remitting MS treated with high efficacy DMTs: Cladribine (CLA, n=11 patients) or Ocrelizumab (OCRE, n=14 patients). The treated patients were compared to control (CTR) untreated subjects (n=15). Blood samples were collected from patients before treatment (time t0) and 6 months post-treatment (time t1), but just once from control subjects. CLA drug tablets were administered to the selected relapsing-remitting MS patients with a dosage of 1.75 mg/kg given for 5 days. OCRE drug was administered to the other relapsing-remitting MS patients by infusion with a dosage of 300 mg, twice in two weeks.

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Microarray based prediction of circular RNA expression in multiple sclerosis

Project description:The aim was to investigate the total circular RNA profile in patients with relapsing–remitting multiple sclerosis and healthy control. We analyzed close to 14,000 individual circRNA per sample.

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Project description:Blood-brain-barrier (BBB) breakdown and active inflammation by relapsing–remitting (RRMS) lesions are hallmarks of multiple sclerosis (MS). Leaky endothelial junctions causes an increased expression of circulating immune cells with associated adhesion molecules on endothelial cell membrane but also an increased production of endothelial derived extracellular microvesicles (EV). Methods: Relapsing–remitting MS (RRMS) patients with no disease-modifying treatment were monitored with weekly intervals using high-resolution 3T MRI scanning. Plasma samples from each measurement were analyzed for protein biomarkers of inflammation by quantitative proteomics, cytokines and chemokines using multiplex immunoassay. Extracellular microvesicles were characterized by an optimized endothelial stress EV Array analysis for detection of soluble secreted microvesicles.

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Homo sapiens

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Alemtuzumab treatment exemplifies discordant immune effects of blood and cerebrospinal fluid in multiple sclerosis

Project description:We here analyzed CSF and blood from two relapsing-remitting multiple sclerosis (RRMS) patients early after peripheral leukocyte depletion with the anti-CD52 antibody alemtuzumab compared to untreated RRMS and control patients using single cell RNA-sequencing.

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Project description:It is fundamentally unknown how normal cellular processes or responses to extracellular stimuli may invoke polyadenylation and degradation of ncRNA substrates or if human disease processes exhibit defects in polyadenylation of ncRNA substrates as part of their pathogenesis. Our results demonstrate that mononuclear cells from subjects with relapsing-remitting multiple sclerosis (RRMS) exhibit pervasive increases in levels of polyadenylated ncRNAs including Y1 RNA, 18S and 28S rRNA, and U1, U2, and U4 snRNAs and these defects are unique to RRMS. Defects in expression of both Ro60 and La proteins in RRMS appear to contribute to increased polyadenylation of ncRNAs. Further, IFN-β1b, a common RRMS therapy, restores both Ro60 and La levels to normal as well as levels of polyadenylated Y1 RNA and U1 snRNA suggesting that aberrant polyadenylation of ncRNA substrates may have pathogenic consequences. We extracted RNA from peripheral whole blood in healthy control subjects and patients with established relapsing-remitting multiple sclerosis using PaxGene tubes.

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