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Newly repopulated spinal cord microglia exhibit a unique transcriptome and contribute to pain resolution (human)

ABSTRACT: Newly repopulated spinal cord microglia exhibit a unique transcriptome and contribute to pain resolution (human)

PROVIDER: PRJNA1046535 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26990784.fastq.gz	Fastqsanger.gz
	SRR26990785.fastq.gz	Fastqsanger.gz
	SRR26990786.fastq.gz	Fastqsanger.gz
	SRR26990787.fastq.gz	Fastqsanger.gz
	SRR26990788.fastq.gz	Fastqsanger.gz

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Newly repopulated spinal cord microglia exhibit a unique transcriptome and contribute to pain resolution

Project description:Microglia contribute to the initiation of pain, however, a translationally viable approach addressing how or when to modulate these cells remains elusive. We used a targeted, inducible, genetic microglial depletion strategy at both acute and acute-to-chronic transition phases in the clinically-relevant tibial fracture/casting pain model to determine the contribution of microglia to the initiation and maintenance of pain. We observed complete resolution of pain which coincided with the timeframe of full repopulation of microglia after transient microglial depletion at the acute-to-chronic phase. These repopulated microglia were morphologically distinct from control microglia, signifying they may exhibit a unique transcriptome. RNA sequencing of repopulated spinal cord microglia identified genes of interest using weighted gene coexpression network analysis (WGCNA). We intersected these genes with a newly generated single nuclei microglial dataset from human spinal cord dorsal horn and identified human-relevant genes that may ultimately promote pain resolution after injury. This work presents a novel approach to gene discovery in pain and provides comprehensive datasets for the development of future microglial-targeted therapeutics.

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Repopulated spinal cord microglia exhibit a unique transcriptome and contribute to pain resolution.

Project description:Microglia are implicated as primarily detrimental in pain models; however, they exist across a continuum of states that contribute to homeostasis or pathology depending on timing and context. To clarify the specific contribution of microglia to pain progression, we take advantage of a temporally controlled transgenic approach to transiently deplete microglia. Unexpectedly, we observe complete resolution of pain coinciding with microglial repopulation rather than depletion. We find that repopulated mouse spinal cord microglia are morphologically distinct from control microglia and exhibit a unique transcriptome. Repopulated microglia from males and females express overlapping networks of genes related to phagocytosis and response to stress. We intersect the identified mouse genes with a single-nuclei microglial dataset from human spinal cord to identify human-relevant genes that may ultimately promote pain resolution after injury. This work presents a comprehensive approach to gene discovery in pain and provides datasets for the development of future microglial-targeted therapeutics.

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