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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE153240 | GEO | 2021/03/17

REPOSITORIES: GEO

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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

Whole-genome gene expression profiling of dorsal root ganglion neurons after nerve damage

Project description:We generated whole-genome gene expression profiles of dorsal root ganglion (DRG) neurons following nerve damage. DRG neurons extend one peripheral axon into the spinal nerve and one central axon into the dorsal root. The peripheral axon regenerates vigorously, while in contrast the central axon has little regenerative capacity. For this study, two groups of animals were subjected either to sciatic nerve (SN) or dorsal root (DR) crush, and at 12, 24, 72 hours and 7 days after the crush, lumbar DRGs L4, L5 and L6 were dissected and total RNA was extracted. For each time point after lesion, three biological replicate RNA samples were hybridized together with the common reference sample consisting of labeld RNA pooled from three unlesioned animals.

2010-09-01 | E-GEOD-21007 | biostudies-arrayexpress

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

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Retinal Ganglion Cell Expression of Cytokine Enhances Occupancy of NG2 Cell-Derived Astrocytes at the Nerve Injury Site: Implication for Axon Regeneration

Project description:Following injuryin the central nervous system, a population of astrocytes occupy the lesion site, form glial bridges and facilitate axon regeneration. Theseastrocytes originate primarily from resident astrocytes orNG2+ oligodendrocyteprogenitor cells. However, theextentto which these cell types give rise to the lesion-filling astrocytes,andwhethertheastrocytes derived from differentcell typescontribute similarly to optic nerve regenerationremain unclear.Here we examine the distributionof astrocytes and NG2+ cellsin an optic nerve crush model.Weshow that optic nerve astrocytes partially fill the injury site over timeafter a crush injury.Viral mediated expression of a growth-promotingfactor,ciliary neurotrophic factor (CNTF),in retinal ganglion cells (RGCs) promotesaxon regeneration without altering the lesion size or the degreeof lesion-filling GFAP+ cells. Strikingly, using inducible NG2Cre driver mice, wefoundthat CNTF overexpression in RGCs increasesthe occupancy ofNG2+ cell-derived astrocytes in the optic nerve lesion. An EdU pulse-chase experiment showsthat the increase in NG2 cell-derived astrocytes is not due to an increase in cell proliferation.Lastly, we performedRNA-sequencing on the injured optic nerve and reveal that CNTF overexpression in RGCs results in significant changes in the expression of distinct genes,including those that encode chemokines, growth factor receptors,and immune cell modulators.Even though CNTF-induced axon regeneration has long been recognized, this is the first evidence of this procedure affecting glial cell fate at the optic nerve crush site.We discuss possible implication of theseresultsforaxon regeneration.

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EE1A1 Interactome

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NIS-lncRNA promotes neuropathic pain by increasing Ccl2 expression

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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

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Gene expression timecourse in zebrafish whole eye in response to optic nerve crush

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