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Sciatic Nerve Injury Triggered Inflammation: Insights into Conditioning-Lesion Induced Axon Regeneration [bulk RNA-seq]

ABSTRACT: Sciatic Nerve Injury Triggered Inflammation: Insights into Conditioning-Lesion Induced Axon Regeneration [bulk RNA-seq]

PROVIDER: PRJNA641848 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12089669_1.fastq.gz	Fastqsanger.gz
	SRR12089669_2.fastq.gz	Fastqsanger.gz
	SRR12089670_1.fastq.gz	Fastqsanger.gz
	SRR12089670_2.fastq.gz	Fastqsanger.gz
	SRR12089671_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Sciatic Nerve Injury Triggered Inflammation: Insights into Conditioning-Lesion Induced Axon Regeneration

Project description:Sciatic Nerve Injury Triggered Inflammation: Insights into Conditioning-Lesion Induced Axon Regeneration

| PRJNA644448 | ENA

Sciatic Nerve Injury Triggered Inflammation: Insights into Conditioning-Lesion Induced Axon Regeneration [bulk RNA-seq]

Project description:Sciatic nerve crush (SNC) triggers sterile inflammation within the distal nerve and deafferented dorsal root ganglia (DRGs). Granulocytes and pro-inflammatory Ly6Chigh monocytes infiltrate the nerve first, and rapidly give way to Ly6C- inflammation-resolving macrophages. Inflammation in DRGs is dominated by tissue resident macrophages, with little contribution from hematogenous leukocytes. Single-cell transcriptomics analysis of injured nerve identified six macrophage subpopulations, repair Schwann cells, and mesenchymal cells as the main cell types. Macrophages at the nerve crush site are distinct from macrophages associated with degenerating nerve fibers. Monocytes and macrophages in the injured nerve “eat” cell corpses of apoptotic leukocytes and thereby promote an anti-inflammatory milieu. Myeloid cells in the injured nerve, but not DRGs, strongly express the receptor for the chemokine GM-CSF. In the absence of GM-CSF, conditioning-lesion induced regeneration of DRG neuron central projections is abolished. Thus, a carefully orchestrated immune response in the nerve is required for conditioning-lesion induced neurorepair.

2021-03-17 | GSE153240 | GEO

Sciatic Nerve Injury Triggered Inflammation: Insights into Conditioning-Lesion Induced Axon Regeneration

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-03-17 | GSE153896 | GEO

Gene expression in mouse DRG neurons at 2 or 5 days post-sciatic lesion in WT and Nfil3-KO

Project description:Mice with a deletion of transcription factor Nfil3 show delayed functional regeneration after sciatic lesion compared to WT mice. To analyze differential gene expression, sciatic nerves were lesioned and nerve endings were coaptated. After two or 5 days, DRGs L4 and L5 were dissected out and gene expression was measured by microarray. Control tissue was taken from the non-injured side. We found that expression of classic regeneration associated genes was similar in WT and Nfil3 KO mice. We did identify a group of differentially expressed genes known for its role in olfactory signal transduction, but were not known as regeneration associated genes until now, which may explain the negative effects on functional recovery. Gene expression in DRGs L4 and L5 from WT and NFIL3 KO mice was analyzed at 2 and 5 days after receiving a sciatic nerve lesion. Control tissue was taken from the non-injured side. Four biological replicates were used per condition. Microarray chips were two color chips, but each channel was analyzed in single color fashion. Conditions were pseudo-randomized over chips in a balanced dye-swap setup.

2015-02-25 | E-GEOD-66259 | biostudies-arrayexpress

Single Cell Atlas of Injured Sciatic Nerve Tissue

Project description:Sciatic nerve crush (SNC) triggers sterile inflammation within the distal nerve and de-afferented dorsal root ganglia (DRGs). In the nerve, neutrophils and pro-inflammatory Ly6Chigh monocytes appear first and rapidly give way to Ly6Clow resolving macrophages. Transcriptional profiling of injured nerve tissue identifies six macrophage subpopulations, repair Schwann cells and mesenchymal cells as the main cell types. Macrophages at the nerve crush site are distinct from macrophages associated with degenerating nerve fibers. Monocytes and macrophages in the injured nerve “eat” apoptotic cell corpses of leukocytes and thereby contribute to an anti-inflammatory milieu. Studies with chimeric mice show that following SNC few blood-derived immune cells enter DRGs. Myeloid cells in the injured nerve, but not DRGs, express the receptor for the chemokine GM-CSF. In the absence of GM-CSF, conditioning-lesion induced regeneration of DRG neuron central projections is abrogated. Thus, a carefully orchestrated immune response in the nerve is required for conditioning-lesion induced neurorepair.

2021-03-17 | GSE153762 | GEO

Clathrin IP_mouse sciatic nerve axons_Roylab_UCSD

Project description:Sciatic nerve axon segments from adult mouse were isolated. Following enzymatic digestion, lysate was subjected to incubation with beads conjugated with either clathrin heavy chain antibody or control IgG antibody for clathrin immunoprecipitation. MudPIT analysis was subsequently performed to identify proteins co-precipitating with clathrin.

2021-08-12 | PXD027857 | Pride

Circadian clock regulator Bmal1 gates axon regeneration via Tet3-5hmC mediated epigenetics

Project description:Axon regeneration of dorsal root ganglia (DRG) neurons after peripheral axotomy involves epigenetic reconfigurations that rewire gene regulatory circuits to establish regenerative gene program. However, the mechanisms and transcriptional regulators remain poorly understood. Here, we conducted an unbiased survey of DNA differentially hydroxymethylated regions (DhMRs) in DRG after peripheral lesion, which identified enriched binding motif for Bmal1, a transcription factor and a central regulator of the circadian clock. Through applying conditional deletion of Bmal1, in vitro and in vivo models of axon regrowth, and transcriptomic profiling, we showed that Bmal1 inhibits axon regeneration in part through Tet3-dependent manner. Mechanistically, Bmal1 functions as a gatekeeper of neuroepigenetic injury responses by limiting Tet3 expression and restricting 5hmC modifications. Notably, Bmal1-regulated genes after axotomy not only concern axon guidance and axon regrowth, but also stress responses, energy homeostasis, and neuroinflammation. Furthermore, we uncovered diurnal oscillation of Tet3 and 5hmC in DRG neurons, and this epigenetic rhythm corresponded to time-of-day effect on axon growth potential. Collectively, our studies showed that Bmal1 deletion mimics the conditioning lesion in lifting epigenetic barriers to enhance axon regeneration.

2023-08-02 | GSE233367 | GEO

Activating injury-responsive genes with hypoxia enhances axon regeneration through neuronal HIF-1α

Project description:Injured peripheral neurons successfully activate a pro-regenerative transcriptional program to enable axon regeneration and functional recovery. How transcriptional regulators coordinate the expression of such programs remains unclear. Here we show that hypoxia-inducible factor 1α (HIF-1α) controls multiple injury-induced genes in sensory neurons and contribute to the pre-conditioning lesion effect. Knockdown of HIF-1α in vitro or conditional knockout in vivo impairs sensory axon regeneration. The HIF-1α target gene Vascular Endothelial Growth Factor A (VEGFA) is expressed in injured neurons and contributes to stimulate axon regeneration. Induction of HIF-1α using hypoxia enhances axon regeneration in vitro and in vivo in sensory neurons. Hypoxia also stimulates motor neuron regeneration and accelerates neuromuscular junction reinnervation. This study demonstrates that HIF-1α represents a critical transcriptional regulator in regenerating neurons and suggests hypoxia as a tool to stimulate axon regeneration.

2016-01-21 | GSE73415 | GEO

Gene expression in mouse DRG neurons at 2 or 5 days post-sciatic lesion in WT and Nfil3-KO

2015-02-25 | GSE66259 | GEO

Epitranscriptomic m6A Regulation of Axon Regeneration in the Adult Mammalian Nervous System

Project description:N6-methyladenosine (m6A) affects multiple aspects of mRNA metabolism and regulates developmental transitions by promoting mRNA decay. Little is known about the role of m6A in the adult mammalian nervous system. Here we report that sciatic nerve lesion elevates levels of m6A-tagged transcripts encoding many regeneration-associated genes and protein translation machinery components in the adult mouse dorsal root ganglion (DRG). Single base resolution m6A-CLIP mapping further reveals a dynamic m6A landscape in the adult DRG upon injury. Loss of either m6A methyltransferase complex component Mettl14 or m6A-binding protein Ythdf1 globally attenuates injury induced protein translation in adult DRGs and reduces functional axon regeneration in the peripheral nervous system in vivo. Furthermore, Pten deletion-induced axon regeneration of retinal ganglion neurons in the adult central nervous system is attenuated upon Mettl14 knockdown. Our study reveals a critical epitranscriptomic mechanism in promoting injury-induced protein synthesis and axon regeneration in the adult mammalian nervous system.

2018-01-17 | GSE106423 | GEO

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