Temporal Changes in Macrophage Phenotype after Peripheral Nerve Injury
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA417027 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6252310.fastq.gz | Fastqsanger.gz | |||
| SRR6252311.fastq.gz | Fastqsanger.gz | |||
| SRR6252312.fastq.gz | Fastqsanger.gz | |||
| SRR6252313.fastq.gz | Fastqsanger.gz | |||
| SRR6252314.fastq.gz | Fastqsanger.gz |
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Project description:Identification of temporal changes in gene expression in macrophages isolated from the site of nerve injury.
2018-06-21 | GSE106488 | GEO
Project description:BACKGROUND:Macrophages play a key role in peripheral nerve repair and demonstrate complex phenotypes that are highly dependent on microenvironmental cues. METHODS:We determined temporal changes in macrophage gene expression over time using RNA sequencing after fluorescence-activated cell sorting (FACS) macrophage populations from injured peripheral nerve. We identified key upstream regulators and dominant pathways using ingenuity pathway analysis and confirmed these changes with NanoString technology. We then investigate the effects of extreme polarizers of macrophage phenotype (IL4 and IFNγ) on nerve regeneration. We determined macrophage gene expression in vivo at the site of peripheral nerve injury with NanoString technology, and assessed recovery from sciatic nerve injury by cranial tibial muscle weights and retrograde labeling motor neurons in mice with deletion of IL4 or IFNγ receptors. RESULTS:We demonstrate that IL4R and IFNγR deletions provide complementary responses to polarization, and alter expression of genes associated with angiogenesis and axonal extension, but do not influence recovery from peripheral nerve transection at 8 weeks after repair. CONCLUSIONS:Overall, this study provides a framework to evaluate the phenotype of macrophages over time, and provides a broader and more precise assessment of gene expression changes than has previously been commonly used. This data suggests ways in which polarization may be modulated to improve repair.
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Project description:Foreign body reaction is one of the most important limiting factors to the clinical translation of implantable bioelectronics. The experiment compares the process of foreign body reaction, following the implantation of a silicon device in a mouse peripheral nerve, to that of peripheral nerve injury, following nerve crushing. Both processes are also compared to a naïve peripheral nerve from an uninjured mouse. The endpoints are day 1, 4, 7, 14 and 28 days.
2022-04-30 | E-MTAB-10294 | biostudies-arrayexpress
Project description:ChIP-seq of H3K27acetylation in sham and injured nerve. Schwann cells play an important role in the response of peripheral nerve to injury. This study was designed to identify enhancers that are altered in sciatic nerve at 3 days post-injury to help identify pathways that mediate the gene expression reprogramming that occurs in Schwann cells after nerve injury. We employed ChIP-seq analysis of H3K27 acetylation as a mark of actively engaged enhancers, and compared enhancers in the distal stump of transected sciatic nerve compared to contralateral (sham) condition.
2014-12-15 | GSE63103 | GEO
Project description:Peripheral nerve injuries are common in modern society. The patients may suffer from partial or total loss of sensory, motor and autonomic function in the involved segments of the body. However, The molecular mechanisms of the regeneration program has not yet been definitively clarified and the comprehensive lncRNA expression signature in peripheral nerve regeneration remains fully unknown.We performed a high throughput microarray assay to detect lncRNA expression profile in the distal end of peripheral nerve at 0,3,7,14 day after injury.
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Project description:Fibro-adipogenic progenitors (FAPs) are muscle-resident mesenchymal progenitors that can contribute to muscle tissue homeostasis and regeneration, as well as postnatal maturation and lifelong maintenance of the neuromuscular system. Recently, traumatic injury to the peripheral nerve was shown to activate FAPs, suggesting that FAPs can respond to nerve injury. However, questions of how FAPs can sense the anatomically distant peripheral nerve injury and whether FAPs can directly contribute to nerve regeneration remained unanswered. Here, utilizing single-cell transcriptomics and mouse models, we discovered that a subset of FAPs expressing GDNF receptors Ret and Gfra1 can respond to peripheral nerve injury by sensing GDNF secreted by Schwann cells. Upon GDNF sensing, this subset becomes activated and expresses Bdnf. FAP-specific inactivation of Bdnf (Prrx1-Cre; Bdnf-fl/fl) resulted in delayed nerve regeneration owing to defective remyelination, indicating that GDNF-sensing FAPs play an important role in the remyelination process during peripheral nerve regeneration. In aged mice, significantly reduced Bdnf expression in FAPs was observed upon nerve injury, suggesting the clinical relevance of FAP-derived BDNF in the age-related delays in nerve regeneration. Collectively, our study revealed the previously unidentified role of FAPs in peripheral nerve regeneration, and the molecular mechanism behind FAPs’ response to peripheral nerve injury.
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Project description:Transcriptional changes are distinct in female and male mice in the time course of peripheral nerve injury response. Here, we present sexually dimorphic transcriptome profiles established in the space of 24 h period after sciatic nerve axotomy.
2022-07-18 | GSE182713 | GEO
Project description:Malignant peripheral nerve sheath tumor (MPNST) is an aggressive sarcoma. Comprehensive proteomic profiles of 23 MPNST tumor specimens were obtained using LC-MS/MS. Among 23 tumor specimens, 13 patients showed favorable prognosis and 10 did local recurrence/distant metastasis.
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Project description:Peripheral nerve injury alters the expression of hundreds of proteins in dorsal root ganglia (DRG). Targeting some of these proteins has led to successful treatments for acute pain, but not for sustained postoperative neuropathic pain. The latter may require targeting multiple proteins. Since a single microRNA (miR) can affect the expression of multiple proteins, here, we describe an approach to identify chronic neuropathic pain-relevant miRs. We used two variants of the spared nerve injury (SNI): Sural-SNI and Tibial-SNI and found distinct pain phenotypes between the two. Both models induced strong mechanical allodynia, but only Sural-SNI rats maintained strong mechanical and cold allodynia, as previously reported. In contrast, we found that Tibial-SNI rats recovered from mechanical allodynia and never developed cold allodynia. Since both models involve nerve injury, we increased the probability of identifying differentially regulated miRs that correlated with the quality and magnitude of neuropathic pain and decreased the probability of detecting miRs that are solely involved in neuronal regeneration. We found seven such miRs in L3-L5 DRG. The expression of these miRs increased in Tibial-SNI. These miRs displayed a lower level of expression in Sural-SNI, with four having levels lower than those in sham animals. Bioinformatics analysis of how these miRs could affect the expression of some ion channels supports the view that, following a peripheral nerve injury, the increase of the 7 miRs may contribute to the recovery from neuropathic pain while the decrease of four of them may contribute to the development of chronic neuropathic pain. The approach used resulted in the identification of a small number of potentially neuropathic pain relevant miRs. Additional studies are required to investigate whether manipulating the expression of the identified miRs in primary sensory neurons can prevent or ameliorate chronic neuropathic pain following peripheral nerve injuries. To identify the miRs that were differentially dysregulated between Tibial-SNI and Sural-SNI, we first performed 12 microarrays in a limited number of samples (in four individual DRGs per group: Sham, Tibial-SNI and Sural-SNI; two L3-DRG and two L4-DRG). Then, miRs identified as having differential expression were corroborated with real time qRT-PCR in RNA isolated from individual DRGs (L3, L4 and L5) derived from 4 rats per group (not presented here, but in the manuscript).
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Project description:Japanese encephalitis (JE) is an acute encephalitis syndrome contributed to Japanese encephalitis virus (JEV) infection. It is the chief cause of viral encephalitis in Asian. In recent years, association of JEV infection with neurological problems such as Guillain-Barré syndrome had reported. Nevertheless, its potential pathogenic mechanism has never been reported. Therefore, it is urgent to explore the relationship between peripheral nerve injury and JEV infection. Here, we use the liquid chromatography-tandem mass spectrometry (LC-MS/MS) technique to make out the protein expression levels of mice sciatic nerve between JEV infection group and the sham group. In general, 4303 proteins were identified by MS, and 187 differentially expressed proteins were found. There were 105 proteins up-regulated in the injured sciatic nerve, and 82 proteins were down-regulated. Functional enrichment analysis of differentially expressed proteins showed that the up-regulated proteins were mainly related to immune regulatory response, and the down-regulated proteins were related to ribosomal structural components and translation.
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