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Major differences in transcriptional alterations in dorsal root ganglia between spinal cord injury and peripheral neuropathic pain models

ABSTRACT: Major differences in transcriptional alterations in dorsal root ganglia between spinal cord injury and peripheral neuropathic pain models

PROVIDER: PRJNA834741 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19052728_1.fastq.gz	Fastqsanger.gz
	SRR19052728_2.fastq.gz	Fastqsanger.gz
	SRR19052729_1.fastq.gz	Fastqsanger.gz
	SRR19052729_2.fastq.gz	Fastqsanger.gz
	SRR19052730_1.fastq.gz	Fastqsanger.gz

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Major differences in transcriptional alterations in dorsal root ganglia between spinal cord injury and peripheral neuropathic pain models

Project description:Chronic, often intractable pain is caused by neuropathic conditions such as peripheral nerve injury (PNI) and spinal cord injury (SCI). These conditions are associated with alterations in gene and protein expression correlated with functional changes in somatosensory neurons having cell bodies in dorsal root ganglia (DRGs). Most studies of DRG transcriptional alterations have utilized PNI models where axotomy-induced changes important for regeneration may overshadow changes that drive neuropathic pain. Both PNI and SCI produce DRG neuron hyperexcitability linked to pain, but contusive SCI produces little peripheral axotomy or peripheral nerve inflammation. Thus, comparison of transcriptional signatures of DRGs across PNI and SCI models may highlight pain-associated transcriptional alterations that don’t depend on peripheral axotomy and associated effects such as peripheral Wallerian degeneration. Data from our rat thoracic SCI experiments were combined with meta-analysis of whole-DRG RNA-seq datasets from prominent rat PNI models. Striking differences were found between transcriptional responses to PNI and SCI, especially in regeneration-associated genes and long noncoding RNAs. Many transcriptomic changes after SCI were also found after corresponding sham surgery, indicating they were caused by injury to surrounding tissue rather than to the spinal cord itself. Another unexpected finding was of few transcriptomic similarities between any rat neuropathic pain model and the only reported transcriptional analysis of human DRGs linked to neuropathic pain. These findings show that DRGs exhibit complex transcriptional responses to central and peripheral neural and tissue injury. Although few genes in DRG cells show similar changes in gene expression across all these painful conditions, the few widely shared transcriptional alterations promise novel insights into fundamental mechanisms within DRGs that can drive neuropathic pain.

2022-10-20 | GSE202111 | GEO

A Transcriptomic Analysis of Neuropathic Pain in Rat Dorsal Root Ganglia Following Peripheral Nerve Injury

Project description:In this study, we screened the differentially expressed genes (DEGs) in the dorsal root ganglia (DRG) from rats with sham or partial sciatic nerve ligation (pSNL) surgery 7 days using RNAseq technique to explore the molecular mechanisms of neuropathic pain

2020-06-30 | GSE117526 | GEO

Microarray analyses of mouse dorsal root ganglia tissue for six different pain models

Project description:Six different mouse pain models were studied: (1) tumour-injection model for bone cancer pain; (2) partial sciatic nerve ligation (PSL) for neuropathic pain; (3) mechanical joint loading for osteoarthritis pain; (4) oxaliplatin-induced painful neuropathy for chemotherapy-induced pain; (5) hyperalgesic priming model for chronic muscle pain; and (6) complete Freund’s adjuvant (CFA)-injection for inflammatory pain. Transcriptomic microarray analyses were performed using RNA isolated from dorsal root ganglia.

2018-06-11 | E-MTAB-6864 | biostudies-arrayexpress

Translational profiling of dorsal root ganglia and spinal cord in a mouse model of neuropathic pain

Project description:Acute pain serves as a protective mechanism, guiding the organism away from actual or potential tissue injury. In contrast, chronic pain is a debilitating condition without any obvious physiological function. The transition to, and the maintenance of chronic pain require new gene expression to support biochemical and structural changes within the pain pathway. The regulation of gene expression at the level of mRNA translation has emerged as an important step in the control of protein expression in the cell. Recent studies show that signaling pathways upstream of mRNA translation, such as mTORC1 and ERK, are upregulated in chronic pain conditions, and their inhibition effectively alleviates pain in several animal models. Despite this progress, mRNAs whose translation is altered in chronic pain conditions remain largely unknown. Here, we performed genome-wide translational profiling of dorsal root ganglion (DRG) and spinal cord dorsal horn tissues in a mouse model of neuropathic pain, spared nerve injury (SNI), using the ribosome profiling technique. We identified distinct subsets of mRNAs that are differentially translated in response to nerve injury in both tissues. We discovered key converging upstream regulators and pathways linked to mRNA translational control and neuropathic pain. Our data are crucial for the understanding of mechanisms by which mRNA translation promotes persistent hypersensitivity after nerve injury.

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HDAC inhibitors attenuate the development of hypersensitivity in models of neuropathic pain [spinal cord tissue]

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. Ipsilateral dorsal spinal cord tissue after L5 spinal nerve transection, DRG tissue was run in a separate Affymetrix experiment.

2013-10-01 | E-GEOD-51294 | biostudies-arrayexpress

Identification of transcript dysregulation in rats with a neuropathic pain, treated or not with vitamin D

Project description:Clinical observations indicate that vitamin D is a pain alleviating molecule. In order to unveil the molecular mechanisms at play, we performed an experimental study on rats with a neuropathic pain. After three weeks of vitamin D treatment, the cerebrum, the spinal cord and the dorsal root ganglia were collected for a transcriptomic analysis, using cDNA microarrays.

2018-04-29 | E-MTAB-6801 | biostudies-arrayexpress

Proteomic Analysis of Spinal Dorsal Horn in Prior-Exercise Protection against Neuropathic Pain

Project description:Neuropathic pain (NP) is a complex and common chronic pain that affects millions of people worldwide. Previous studies showed that prior exercise protects against NP caused by nerve injury, but the mechanisms remain elusive. Therefore, this study aimed to identify the differentially expressed proteins (DEPs) involved in the process of protecting against NP by prior exercise and explore the underlying mechanisms through bioinformatic analysis.

2025-05-07 | PXD054342 | Pride

mRNA expression profiling in the spinal nerve ligation model of neuropathic pain in rats

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

2011-10-18 | GSE24982 | GEO

GPR37L1 identifies spinal cord astrocytes and protects neuropathic pain after nerve injury

Project description:Astrocytes in the spinal cord dorsal horn (SDH) play a pivotal role in synaptic transmission and neuropathic pain. However, the precise classification of SDH astrocytes in health and disease remains elusive. Here we reveal Gpr37l1 as a marker and functional regulator of spinal astrocytes. Through single-nucleus RNA sequencing, we identified Gpr37l1 as a selective GPCR marker for spinal cord astrocytes. Notably, SDH displayed reactive astrocyte phenotypes and exacerbated neuropathic pain following nerve injury combined with Gpr37l1 deficiency. In naïve animals, GPR37L1 knockdown in SDH astrocytes induces astrogliosis and pain hypersensitivity, while Gpr37l1-/- mice fail to recover from neuropathic pain. GPR37L1 activation by maresin-1 increased astrocyte GLT-1 activity and reduced spinal EPSCs and neuropathic pain. Selective overexpression of Gpr37l1 in SDH astrocytes reversed neuropathic pain and astrogliosis after nerve injury. Our findings illuminate astrocyte GPR37l1 as an essential negative regulator of pain, which protects neuropathic pain through astrocyte signaling in SDH.

2025-02-14 | GSE286467 | GEO

Translational profiling of dorsal root ganglia and spinal cord in a mouse model of neuropathic pain

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