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DNA methylation reprogramming after spinal nerve injury [RRBS]

ABSTRACT: DNA methylation reprogramming after spinal nerve injury [RRBS]

PROVIDER: PRJNA472956 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7213190.fastq.gz	Fastqsanger.gz
	SRR7213191.fastq.gz	Fastqsanger.gz
	SRR7213192.fastq.gz	Fastqsanger.gz
	SRR7213193.fastq.gz	Fastqsanger.gz
	SRR7213188.fastq.gz	Fastqsanger.gz

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DNA methylation reprogramming after spinal nerve injury [RRBS]

Project description:Purpose: Nerve injury-induced hyperactivity of primary sensory neurons in the dorsal root ganglion (DRG) contributes critically to chronic pain development, but its underlying mechanisms remain incompletely understood. Chronic neuropathic pain has a clear epigenetic component, however, most studies so far have focused on histone modifications. We determined changes of DNA methylation in the rat DRG, spinal cord, and prefrontal cortex after spinal nerve ligation (SNL).

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DNA methylation reprogramming after spinal nerve injury

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Discovery of potential candidate proteins reprogramming spinal cord derived astrocytes into neurons by proteomic analysis

Project description:Spinal cord injury (SCI) is a common but devastating trauma of the central nerve system. In this study, we reprogrammed cultured spinal-cord reactive astrocytes into neurons by Neurod1 expression. The mechanism of programmed conversion from astrocytes to neurons has not been clarified yet. Thus, we used label-free proteomics to identify differentially expressed proteins in Neurod1 over-expressed astrocytes and control group. A total of 1952 proteins were identified, including 92 significantly changed proteins. Among these proteins, 8 proteins were identified as candidates involving in the process of the reprogramming, based on their biological function and fold change in the bioinformatic analysis. Our study revealed that that Neurod1 can directly reprogram cultured spinal-cord reactive astrocytes into neurons, and several proteins that could play a significant role during the neuronal reprogramming were discovered.

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Sex-specific transcriptome of spinal microglia in neuropathic pain due to peripheral nerve injury

Project description:Neuropathic pain is a prevalent and debilitating chronic disease that is characterized by activation in glial cells in various pain-related regions within the central nervous system. Recent studies have suggested a sexually dimorphic role of microglia in the maintenance of neuropathic pain in rodents. Here, we utilized RNA sequencing analysis of microglia to identify whether there is a common neuropathic microglial signature and characterize the sex differences in microglia in pain-related regions in nerve injury and chemotherapy-induced peripheral neuropathy mouse models. Whilst mechanical allodynia and behavioral changes were observed in all models, transcriptomic analysis of microglia revealed no common transcriptional changes in spinal and supraspinal regions and in different neuropathic models. However, there was a substantial change in microglial gene expression within the ipsilateral lumbar spinal cord 7-days after chronic constriction injury (CCI) of the sciatic nerve. Both sexes upregulated genes associated with inflammation, phagosome, and lysosome activation, though males revealed a prominent global transcriptional shift not observed in female mice. This study demonstrates a lack of a common neuropathic microglial signature and indicates distinct sex differences in spinal microglia, suggesting they contribute to the sex-specific pain processing following nerve injury.

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