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.
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.
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.
Project description:We analyzed the transcriptome profile of B cells from patients with relapsing-remitting multiple sclerosis (RRMS), patients with primary progressive multiple sclerosis (PPMS) and healthy individuals. High-density Clariom D Arrays for human were used to quantify the transcript levels. This GEO entry provides the processed Clariom D microarray data from the gene-level and exon-level workflows.
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.
Project description:The purpose of this study was to characterize the transcriptional effects induced by intramuscular IFN-beta-1a treatment (Avonex, 30 µg once weekly) in patients with relapsing-remitting form of multiple sclerosis (MS). By using Affymetrix DNA microarrays, we obtained genome-wide expression profiles of peripheral blood mononuclear cells from 24 MS patients within the first four weeks of IFN-beta administration. Keywords: Multiple sclerosis, Interferon, Pharmacogenomics, Affymetrix
