Gene expression change in the lingual nerve and the traumatic neuromas after the injured lingual nerve.
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ABSTRACT:
PROVIDER: PRJNA513034 | ENA |
REPOSITORIES: ENA
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Project description:The lingual nerves are incidentally injured in many oral and maxillofacial surgical procedures, traumatic neuroma was observed at the proximal stump of the injured lingual nerve in patients with severe lingual nerve disturbance. Various genes including genes related to nerve regeneration are expressed in the rat and mouse traumatic neuroma, as regeneration mechanism works after lingual nerve injury. Few reported have showed the expressed genes in the traumatic neuroma of the human lingual nerve. In this study, we compared the gene expression between pooled RNA sample from three traumatic neuromas removed in microneurosurgery in the lingual nerve and an RNA sample from the normal lingual nerve on the unaffected side of the removed tongue with cancer. The 2,357 genes increased more than twofold in the traumatic neuroma compared with the normal lingual nerve. Then, we analyzed the upregulated genes in DAVID and DAVID indicated that the 20 upregulated genes were associated with protein secretion to the extracellular space in the pathways. This study identified the 20 candidate genes at the nerve regeneration stage in the traumatic neuroma in the human lingual nerve.
2022-01-04 | GSE124668 | GEO
Project description:Injured Sciatic Nerve Atlas (iSNAT)
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Project description:ChIP-seq of c-JUN in injured rat peripheral nerve
2022-03-01 | GSE190858 | GEO
Project description:Proteomic analysis of injured human peripheral nerves, particularly focusing on events occurring in the proximal and distal nerve ends, remains relatively underexplored. This study aimed to investigate the molecular patterns underlying a digital nerve injury, concentrating on differences in protein expression between the proximal and distal nerve ends. A total of 26 human injured digital nerve samples (24 men; 2 women; median age 47 [30-66] years), harvested during primary nerve repair within 48 hours post-injury from proximal and distal nerve ends, were analyzed using mass spectrometry. A total of 3914 proteins were identified, with 127 proteins showing significant differences in abundance between the proximal and the distal nerve ends. The downregulation of proteins in the distal nerve end was associated with synaptic transmission, autophagy, neurotransmitter regulation, cell adhesion and migration. Conversely, proteins upregulated in the distal nerve end were implicated in cellular stress response, neuromuscular junction stability and muscle contraction, neuronal excitability and neurotransmitter release, synaptic vesicle recycling and axon guidance and angiogenesis. Investigation of proteins, with functional annotations analysis, in proximal and the distal ends of human injured digital nerves, revealed dynamic cellular responses aimed at promoting tissue degeneration and restoration, while suppressing non-essential processes.
2024-07-19 | PXD051266 | Pride
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.
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Project description:Single Cell Atlas of Injured Sciatic Nerve Tissue
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Project description:The goal of the experiment was to determine the role of the polycomb repressive complex 2 in the nerve injury response in peripheral nerve. A Schwann cell specific knockout of the Eed subunit of PRC2 was generated to compare with wild type mice in sham and injured mice at 1d and 14d timepoints after nerve injury.
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Project description:Endothelial cells-derived extracellular vesicles can promote nerve function in mice with traumatic brain injury. We used snRNAseq to analyze the effects of extracellular vesicles derived from endothelial cells on nerve cells in mice with traumatic brain injury.
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Project description:Peripheral nerves provide a supportive growth environment for developing and regenerating axons and are essential for maintenance and repair of many non-neural tissues. This capacity has largely been ascribed to paracrine factors secreted by nerve-resident Schwann cells. Here, we used single-cell transcriptional profiling to identify ligands made by different injured rodent nerve cell types and have combined this with cell-surface mass spectrometry to computationally model potential paracrine interactions with peripheral neurons. These analyses show that peripheral nerves make many ligands predicted to act on peripheral and CNS neurons, including known and previously uncharacterized ligands. While Schwann cells are an important ligand source within injured nerves, more than half of the predicted ligands are made by nerve-resident mesenchymal cells, including the endoneurial cells most closely associated with peripheral axons. At least three of these mesenchymal ligands, ANGPT1, CCL11, and VEGFC, promote growth when locally applied on sympathetic axons. These data therefore identify an unexpected paracrine role for nerve mesenchymal cells and suggest that multiple cell types contribute to creating a highly pro-growth environment for peripheral axons.
2020-05-06 | GSE146883 | GEO