A transcriptome data set for comparing skin, muscle and DRG between acute and chronic postsurgical pain rats.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1112900 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29070300_1.fastq.gz | Fastqsanger.gz | |||
| SRR29070300_2.fastq.gz | Fastqsanger.gz | |||
| SRR29070301_1.fastq.gz | Fastqsanger.gz | |||
| SRR29070301_2.fastq.gz | Fastqsanger.gz | |||
| SRR29070302_1.fastq.gz | Fastqsanger.gz |
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Project description:Chronic postsurgical pain (CPSP), with a high prevalence and rising epidemic of opioids crisis, is typically derived from acute postoperative pain. Revealing the peripheral mechanisms behind the transition from acute to chronic pain after surgery is necessary. We established on two recognized animal models, the Lateral Paw Incision (LPI) model and the Skin/Muscle Incision and Retraction (SMIR) model, in simulation of acute and chronic postsurgical pain. The tissue of incisional skin, muscle and DRG at several time points are harvested and send for next-generation RNA sequencing (RNA-seq). Then the quality of sequencing results is validated. Our data could explain the time-course transcriptomic variation in the tissue of skin, muscle and DRG, and further to identify the potential origin and mechanism of CPSP.
2024-10-08 | GSE267799 | GEO
Project description:Expression profiling of L4 and L5 Dorsal Root Ganglion (DRG) in the spinal nerve ligation model of neuropathic pain. The goal of the study was to identify genes involved in neuropathic pain This series of samples comprises of contralateral and ipsilateral L4 and L5 DRG tissue collected 4 weeks after rats underwent a L5 spinal nerve ligation (SNL) or a sham operation with no L5 spinal nerve ligation. This defines 8 groups (i) contralateral L4 DRG from the sham cohort (n=5), (ii) ipsilateral L4 DRG from sham cohort (n=5), (iii) contralateral L4 DRG from SNL cohort (n=5), (iv) ipsilateral L4 DRG from the SNL chort (n=5), (v) contralateral L5 DRG from the sham cohort (n=5), (vi) ipsilateral L5 DRG from sham cohort (n=5), (vii) contralateral L5 DRG from SNL cohort (n=5), (viii) ipsilateral L5 DRG from the SNL cohort (n=5)
2011-10-17 | E-GEOD-24982 | biostudies-arrayexpress
Project description:We found that intrathecal injection of anthrax edema toxin (ET), causes analgesia in adult B6J mice. In order to determine if DRG neuron transcriptional responses play a role in pain blockade, we performed a bulk RNA-seq experiment on dissected mouse DRG neurons. We report that anthrax edema toxin causes transcriptional responses in DRG neurons 2h after in vivo administration
2021-09-29 | GSE184619 | GEO
Project description:Functionally distinct subtypes/clusters of dorsal root ganglion (DRG) neurons may play different roles in nerve regeneration and pain. However, details about their transcriptomic changes under neuropathic pain conditions remain unclear. Chronic constriction injury (CCI) of the sciatic nerve represents a well-established model of neuropathic pain, and we conducted single-cell RNA-sequencing (scRNA-seq) to characterize subtype-specific perturbations of transcriptomes in lumbar DRG neurons on day 7 post-CCI. By using PirtEGFPf mice that selectively express an enhanced green fluorescent protein in DRG neurons, we established a highly efficient purification process to enrich neurons for scRNA-seq. We observed the emergence of four prominent CCI-induced clusters and a loss of marker genes in injured neurons. Importantly, a portion of injured neurons from several clusters were spared from injury-induced identity loss, suggesting subtype-specific transcriptomic changes in injured neurons. Moreover, uninjured neurons, which are necessary for mediating the evoked pain, also demonstrated cell-type-specific transcriptomic perturbations in these clusters, but not in others. Notably, male and female mice showed differential transcriptomic changes in multiple neuronal clusters after CCI, suggesting transcriptomic sexual dimorphism in DRG neurons after nerve injury. Using Fgf3 as a proof-of-principle, RNAscope study provided further evidence of increased Fgf3 in injured neurons after CCI, supporting scRNA-seq analysis, and calcium imaging study unraveled a functional role of Fgf3 in neuronal excitability. These findings may contribute to the identification of new target genes and the development of DRG neuron cell-type-specific therapies for optimizing neuropathic pain treatment and nerve regeneration.
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Project description:Objective: The diagnostic roles of long non-coding RNAs (lncRNAs) and mRNAs in bone cancer pain are still not well defined. We aimed to identify differentially expressed DRG mRNAs in bone cancer pain and sham group rats systematically. Methods: Expression profile of mRNAs in DRG from bone cancer pain and sham group rats was analyzed by microarray assay. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway based approaches were used to investigate biological functions and signaling pathways affected by the differentially expressed mRNAs. GPR160 was selected for validation using Real-Time PCR. Results: Compared with sham group, a total of 807 differentially expressed mRNAs were revealed by heatmap and volcano-plot, including up-regulation in 720 and down-regulation in 87 (fold change ≥ 2 and P < 0.05), respectively. Pathways analysis based on upregulated mRNAs were mainly involved in antigen processing and presentation and phagosome pathway (P < 0.05). We first reported differentially expressed mRNAs in bone cancer pain and sham group rats systemically. Combined with the published dataset, we identified several differentially expressed mRNAs which might to be diagnostic or prognostic markers. The biological functions of those mRNAs should be further validated. Taken together, this study provided the basis for future treatment of bone cancer pain.
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Project description:This program addresses the gene signature associated with DRG in the Chung rat model for neuropathic pain. The Chung neuropathic pain profiling data was analyzed by identifying genes that were up- and down-regulated at selected p value and fold change in DRG of the Sprague Dawley rats following spinal nerve ligation compared to the sham-operated controls.
2013-03-22 | E-GEOD-38038 | biostudies-arrayexpress
Project description:Histone deacetylase inhibitors (HDACIs) interfere with the epigenetic process of histone acetylation and are known to have analgesic properties in models of chronic inflammatory pain. The aim of this study was to determine whether these compounds could also affect neuropathic pain. Different class I HDACIs were delivered intrathecally into rat spinal cord in models of traumatic nerve injury and antiretroviral drug-induced peripheral neuropathy (stavudine, d4T). Mechanical and thermal hypersensitivity was attenuated by 40% to 50% as a result of HDACI treatment, but only if started before any insult. The drugs globally increased histone acetylation in the spinal cord, but appeared to have no measurable effects in relevant dorsal root ganglia in this treatment paradigm, suggesting that any potential mechanism should be sought in the central nervous system. Microarray analysis of dorsal cord RNA revealed the signature of the specific compound used (MS-275) and suggested that its main effect was mediated through HDAC1. Taken together, these data support a role for histone acetylation in the emergence of neuropathic pain. n = 4, HDACi treated vs. vehicle treated. Injured ipsilateral DRG after L5 spinal nerve transection. Spinal cord tissue was run in a separate Affymetrix experiment.
2013-10-01 | E-GEOD-51295 | biostudies-arrayexpress
Project description:Inflammation plays a role in neuropathic pain conditions as well as in pain induced solely by an inflammatory stimulus. Robust mechanical hyperalgesia and allodynia can be induced by locally inflaming the L5 dorsal root ganglion (DRG) in rat. This model allows investigation of the contribution of inflammation per se to chronic pain conditions. Most previous microarray studies of DRG gene expression have investigated neuropathic pain models involving axon transection. To examine the role of inflammation, we used microarray methods to examine gene expression 3 days after local inflammation of the L5 DRG in rat. We observed significant regulation in a large number of genes (23% of observed transcripts), and examined 221 (3%) with a fold-change of 1.5-fold or more in more detail. Immune-related genes were the largest category in this group and included members of the complement system as well as several pro-inflammatory cytokines. However, these upregulated cytokines had no prior links to peripheral pain in the literature other than through microarray studies, though most had previously described roles in CNS (especially neuroinflammatory conditions) as well as in immune responses. The L5 dorsal root ganglion (DRG) was locally inflamed with zymosan/Incomplete Freund's Adjuvant. DRG were isolated 3 days later. Each sample was RNA extracted from a single DRG. 6 samples from rats with local DRG inflammation were compared with 6 samples from sham-operated rats.
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Project description:Two out-bred rat selection lines were separated to produce different hypersensitivity phenotypes following nerve injury. These lines were termed High Pain and Low Pain (HP or LP). Each sub-strain was either subject to a Sham surgery or a Spinal Nerve Ligation (SNL) surgery to the L4 and L5 spinal nerves. Three days following surgery L4/L5 Dorsal Root Ganglia (DRG) were dissected from these animals. For the rat line separation protocol see: Devor M, Raber P (1990) Heritability of symptoms in an experimental model of neuropathic pain. Pain 42:51-67. 12 Hybridizations, 3 per condition; Sham HP DRG; 3 day SNL HP DRG; Sham LP DRG; 3 day SNL LP DRG.
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