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Maresin-1 promotes neuroprotection in relapsing remitting mouse model of multiple sclerosis

ABSTRACT: Maresin-1 promotes neuroprotection in relapsing remitting mouse model of multiple sclerosis

PROVIDER: PRJNA1159147 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30618490_1.fastq.gz	Fastqsanger.gz
	SRR30618490_2.fastq.gz	Fastqsanger.gz
	SRR30618491_1.fastq.gz	Fastqsanger.gz
	SRR30618491_2.fastq.gz	Fastqsanger.gz
	SRR30618492_1.fastq.gz	Fastqsanger.gz

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Maresin-1 promotes neuroprotection in relapsing remitting mouse model of multiple sclerosis

Project description:Multiple sclerosis (MS) is a prevalent inflammatory neurodegenerative disease in young people, causing neurological abnormalities and impairment. We investigated the effect of maresin 1 (MaR1) on the progression of disease in relapsing remitting form of experimental autoimmune encephalomyelitis (RR-EAE). Treatment with MaR1 in RR-EAE accelerated inflammation resolution, protected against neurological impairments, and delayed disease development by reducing immune cell infiltration (CD4+IL17+ and CD4+IFNg+) into the CNS. Furthermore, injection of MaR1 enhanced IL-10 production, primarily in macrophages and CD4+ cells. However, neutralizing IL-10 with an anti-IL-10 antibody eliminated MaR1's protective impact on RR-EAE, implying that IL-10 plays a role in MaR1's EAE protection. Metabolism is increasingly being recognized as a critical element controlling the effector activity of many immune cells. Our investigation found that, when compared to vehicle treatment, MaR1 administration significantly repaired the metabolic dysregulation seen in CD4+ cells, macrophages, and microglia in the treated group. Furthermore, MaR1 treatment restored defective efferocytosis in EAE mice, which was potentially facilitated by the induction of metabolic alterations in macrophages and microglia. MaR1 also preserved myelin in the EAE group and regulated O4+ oligodendrocyte metabolism by reversing metabolic dysregulation via increased mitochondrial activity and decreased glycolysis. Overall, in a preclinical MS animal model, MaR1 therapy has anti-inflammatory and neuroprotective properties. It also induced metabolic reprogramming in disease-associated cell types, increased efferocytosis, and maintained myelination. These findings suggest MaR1's potential as a novel therapeutic agent for MS and other autoimmune diseases

2024-12-08 | GSE276812 | GEO

Defective structural RNA processing in relapsing-remitting multiple sclerosis

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.

2015-03-10 | E-GEOD-66573 | biostudies-arrayexpress

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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Defective structural RNA processing in relapsing-remitting multiple sclerosis

2015-03-10 | GSE66573 | GEO

Double-stranded Alu RNAs, type 1 IFN responses, and relapsing remitting multiple sclerosis

Project description:Double-stranded Alu RNAs, type 1 IFN responses, and relapsing remitting multiple sclerosis

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Therapeutic efficacy of dimethyl fumarate in relapsing-remitting multiple sclerosis is linked with monocytic oxidative responses [Illumina]

Project description:Dimethyl fumarate (DMF) is a first-line-treatment for relapsing-remitting multiple sclerosis (RRMS). The redox master regulator Nrf2, essential in redox balance, is a target of DMF, but the precise therapeutic mechanisms remain elusive. Here we show impact of DMF on circulating monocytes and T cells in a prospective longitudinal RRMS patient cohort. DMF increased the level of oxidized isoprostanes in peripheral blood. Other observed changes, including methylome and transcriptome profiles, occur in monocytes prior to T cells. Importantly, monocyte counts and monocytic ROS increase following DMF and distinguish patients with beneficial treatment-response from non-responders. A single nucleotide polymorphism in the ROS-generating NOX3 gene is associated with beneficial DMF treatment-response and suggestively associated with increased ROS generation. Our data implicate monocyte-derived oxidative processes in autoimmune diseases and their treatment, and identify NOX3 genetic variant, monocyte counts and redox state as parameters potentially useful to inform clinical decisions on DMF therapy of RRMS.

2019-07-31 | GSE130491 | GEO

Therapeutic efficacy of dimethyl fumarate in relapsing-remitting multiple sclerosis is linked with monocytic oxidative responses [Affymetrix]

2019-07-31 | GSE130478 | GEO

Therapeutic efficacy of dimethyl fumarate in relapsing-remitting multiple sclerosis is linked with monocytic oxidative responses

Project description:Therapeutic efficacy of dimethyl fumarate in relapsing-remitting multiple sclerosis is linked with monocytic oxidative responses

| PRJNA540471 | ENA

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

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

| PRJNA957301 | ENA

Therapeutic efficacy of dimethyl fumarate in relapsing-remitting multiple sclerosis is linked with monocytic oxidative responses [Illumina]

Project description:Therapeutic efficacy of dimethyl fumarate in relapsing-remitting multiple sclerosis is linked with monocytic oxidative responses [Illumina]

| PRJNA540475 | ENA

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