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Transcriptomes in the Sciatic Nerves of Lewis Rats with Experimental Autoimmune Neuritis

ABSTRACT: Transcriptomes in the Sciatic Nerves of Lewis Rats with Experimental Autoimmune Neuritis

PROVIDER: PRJNA552457 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9639750_1.fastq.gz	Fastqsanger.gz
	SRR9639750_2.fastq.gz	Fastqsanger.gz
	SRR9639760_1.fastq.gz	Fastqsanger.gz
	SRR9639760_2.fastq.gz	Fastqsanger.gz
	SRR9639751_1.fastq.gz	Fastqsanger.gz

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Transcriptomes in the Sciatic Nerves of Lewis Rats with Experimental Autoimmune Neuritis

Project description:Guillain-Barré syndrome (GBS) is characterized by acute immune-mediated peripheral neuropathy, which may result in rapidly progressive paralysis and fatal respiratory failure. As the underlying pathological mechanisms of GBS are unclear, we surveyed the transcriptome of rats with experimental autoimmune neuritis (EAN), a model of GBS. Briefly, sciatic nerves on both sides were collected from 8–10-week-old Lewis rats during early (10 days post-induction), peak (19 days), and late neuritis (30 days). Total RNA was sequenced to identify differentially expressed genes. Compared to control rats without induced neuritis, 33 genes were differentially expressed in the early phase (14 upregulated and 19 downregulated), with an adjusted P-value < 0.05 and |log2 fold-change| > 1, as were 137 genes in the peak phase (126 upregulated and 11 downregulated) and 60 genes in the late phase (58 upregulated and 2 downregulated). Eleven of these genes were common to all stages, suggesting their crucial roles throughout the disease course. Analysis of protein-protein interactions revealed Fos, Ccl2, Itgax and C3 as node genes at different stages. Functional analysis of differentially expressed genes identified biological processes and pathways that are activated as neuritis progresses. This is the first genome-wide gene expression study of peripheral nerves in experimental autoimmune neuritis model. Dynamic gene expression and significantly altered biological functions were detected in different phases of the disease, increasing our understanding of the molecular mechanisms underlying EAN and highlighting potential targets for its diagnosis and treatment.

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