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Mus musculus

ABSTRACT: Analysis of the host transcriptome from demyelinating spinal cord of murine coronavirus infected mice

PROVIDER: PRJNA189553 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR725546.fastq.gz	Fastqsanger.gz
	SRR725547.fastq.gz	Fastqsanger.gz

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Analysis of the host transcriptome from demyelinating spinal cord of murine coronavirus infected mice

Project description:We use transcriptome analysis to study the spinal cord transcriptome during MHV-induced demyelinating disease and find important biological pathways for demyelinating pathology. We find evidence of a Th1 cytokine response, ongoing antigen presentation and lymphocyte proliferation, lipid metabolism changes, and eicosanoid inflammation. In addition, we report several genes important for osteoclast function have augmented expression in the CNS during demyelination, suggesting a parallel between the osteoclast and microglial functions in maintaining homeostasis and the fidelity of specialized extracellular matrices in their respective compartments. RNA-seq of mock-infected and MHV-infected spinal cord tissue at 33 days post-infection, the peak of demyelination.

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Intranasal therapy with miRNA-219 reduces viral load and encephalomyelitis in the TMEV model of multiple sclerosis

Project description:Purpose: RNA sequencing of spinal cord following intranasal administration of miRNA-219 in Theiler’s murine encephalomyelitis virus (TMEV) model of multiple sclerosis Methods: RNA isolated from spinal cords was analyzed by Next-Generation RNA Sequencing (Illumina) Results: Here, we analyzed the therapeutic effects of miR-219 in a virus-induced demyelinating model. Following intranasal administration of miR-219 in TMEV-infected mice, we found significant reduction of clinical signs, virus persistence (virus genome copy numbers), neuroglia activation, proinflammatory cytokine levels, and demyelination. RNA sequencing of expressed host genes demonstrated that miR-219 potentiates transcriptional changes in cholesterol-related genes, leading to reduced levels of this lipid. Conclusions: Since virus replication relies on hijacking cholesterol biosynthesis and trafficking of host cell endogenous pools as well as remodeling intracellular membranes, i.e., the virus replication organelles or viroplasm, treatment with miR-219 may interfere with virus RNA replication through downregulation of cholesterol synthesis. Our findings show that miR-219 administration lessens pathological changes by reducing the CNS virus loads and favoring myelin repair.

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