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DNA methylation reprogramming after spinal nerve injury [RRBS]

ABSTRACT: Purpose: Nerve injury-induced hyperactivity of primary sensory neurons in the dorsal root ganglion (DRG) contributes critically to chronic pain development, but its underlying mechanisms remain incompletely understood. Chronic neuropathic pain has a clear epigenetic component, however, most studies so far have focused on histone modifications. We determined changes of DNA methylation in the rat DRG, spinal cord, and prefrontal cortex after spinal nerve ligation (SNL).

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE114865 | GEO | 2018/07/05

REPOSITORIES: GEO

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DNA methylation reprogramming after spinal nerve injury

Project description:Purpose: Nerve injury-induced hyperactivity of primary sensory neurons in the dorsal root ganglion (DRG) contributes critically to chronic pain development, but its underlying mechanisms remain incompletely understood. Chronic neuropathic pain has a clear epigenetic component, however, most studies so far have focused on histone modifications. We determined changes of DNA methylation in the rat DRG, spinal cord, and prefrontal cortex after spinal nerve ligation (SNL).

2018-06-29 | GSE100641 | GEO

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 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

A novel functional role for the serine protease inhibitor SerpinA3N and its substrate leukocyte elastase in neuropathic pain

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.

2015-02-19 | E-GEOD-63442 | biostudies-arrayexpress

RNA-seq of rat dorsal root ganglia after ligation to investigate central nervous system transcriptomics in chronic pain using agnostic splice site discovery methods

Project description:The study pursued dual goals: To advance mRNA-seq bioinformatics towards unbiased transcriptome capture and to demonstrate its potential for discovery in neuroscience by applying the approach to an in vivo model of neurological disease. We found that 12.4% of known genes were induced and 7% were suppressed in the dysfunctional (but anatomically intact) L4 dorsal root ganglion (DRG) 2 weeks after L5 spinal Nerve Ligation (SNL). A new algorithm for agnostic mapping of pre-mRNA splice junctions (SJ) achieved a precision of 97%. mRNA-seq of L4 DRG 2 weeks and 2 months after L5 spinal nerve ligation. CONTROL and SNL were used to identify differential gene expression between chronic pain and standard conditions in Rattus norvegicus. CONTROL and SNL and PILOT were used to perform 'agnostic splice site discovery' in the nervous system transcriptome in Rattus norvegicus

2010-05-01 | E-GEOD-20895 | biostudies-arrayexpress

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

2011-10-18 | GSE24982 | GEO

A novel functional role for the serine protease inhibitor SerpinA3N and its substrate leukocyte elastase in neuropathic pain

2015-02-19 | GSE63442 | GEO

Profiling Chung rat model for neuropathic pain

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

Gene expression signatures for lumber 5 dorsal horn of spinal cord in spinal nerve ligation (SNL) mice with WTD intervention

Project description:For development of gene expression of L5 spinal tissue in SNL mice, L5 spinal nerve was first tightly ligated to construct the neuropathic pain model, and sham-operated group as a control. After chronic administrations of vehicle (distilled water, 10 mg/kg) or WTD (12.60 g/kg, p.o.), L5 spinal cord of dorsal horn were collected, and then, Agilent Whole Mouse Genome Microarray 4×44K expression profiling were employed as a discovery platform to identify genes with the potential to provide basis for the clinical application of WTD for neuropathic pain. A 579-gene consensus signature was identified that distinguished between sham and SNL samples, and a 456-gene consensus signature was identified that distinguished between WTD and SNL samples. Expression of 12 genes (Crk1, Fgf13, Fgfr1, Crk1, Adrbk1, Erbb3, Gnas, Vegfa, Crk1, Erbb3, Drd2, Gnas) were identified as the efficacy of differentially expressed genes.

2017-03-28 | GSE97076 | GEO

mTOR-neuropeptide Y signaling sensitizes nociceptors to drive neuropathic pain development

Project description:Neuropathic pain is a refractory condition that involves de novo protein synthesis in the nociceptive pathway. The mechanistic target of rapamycin (mTOR) is a master regulator of protein synthesis; however, mechanisms underlying its role in neuropathic pain remain elusive. Using spared nerve injury-induced neuropathic pain model, we found mTOR activation in large-diameter dorsal root ganglion (DRG) neurons and spinal microglia. However, selective ablation of mTOR in DRG neurons, rather than microglia, alleviated neuropathic pain. Combining transcriptomic profiling, electrophysiological recording and pharmacologic manipulations, we demonstrated that activated mTOR promoted neuropeptide Y (NPY) induction in mechanoreceptors and that NPY acted on Y2 receptors (Y2R) but not Y1R to enhance nociceptor excitability. Peripheral replenishment of NPY reversed pain alleviation upon mTOR removal, whereas Y2R antagonists prevented its function. Our findings reveal an unexpected link between mTOR and NPY in promoting nociceptor sensitization and neuropathic pain, through NPY/Y2R signaling-mediated intra-ganglionic transmission.

2022-09-01 | GSE184014 | GEO

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.

2018-12-18 | GSE123919 | GEO

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