Differential DNA Methylation in the PFC across the transition from acute to chronic pain
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ABSTRACT:
PROVIDER: PRJNA609721 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11214900_1.fastq.gz | Fastqsanger.gz | |||
| SRR11214900_2.fastq.gz | Fastqsanger.gz | |||
| SRR11214901_1.fastq.gz | Fastqsanger.gz | |||
| SRR11214901_2.fastq.gz | Fastqsanger.gz | |||
| SRR11214902_1.fastq.gz | Fastqsanger.gz |
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Project description:We performed genome-wide bisulfite capture sequencing in prefrontal cortex in male mice at four timepoints (one day, two weeks, six months, and one year) post-neuropathic injury in order to track and observe dynamics of DNA methylation and epigenetic regulation in response to the development of chronic pain. We identified hundreds of differentially methylated CpGs and genes at FDR < 0.1 and differential methylation > 5%. PFC DNA methylation rapidly and robustly responds to neuropathic injury and genes display time point specific patterns of differential methylation.
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Project description:Not all patients with nerve injury develop neuropathic pain. The extent of nerve damage and age at the time of injury are two of the few risk factors identified to date. In addition, preclinical studies show that neuropathic pain variance is heritable. To define such factors further, we performed a large-scale gene profiling experiment which plotted global expression changes in the rat dorsal root ganglion in three peripheral neuropathic pain models. This resulted in the discovery that the potassium channel alpha subunit KCNS1, involved in neuronal excitability, is constitutively expressed in sensory neurons and markedly downregulated following nerve injury. KCNS1 was then characterized by an unbiased network analysis as a putative pain gene, a result confirmed by single nucleotide polymorphism association studies in humans. A common amino acid changing allele, the 'valine risk allele', was significantly associated with higher pain scores in five of six independent patient cohorts assayed (total of 1359 subjects). Risk allele prevalence is high, with 18-22% of the population homozygous, and an additional 50% heterozygous. At lower levels of nerve damage (lumbar back pain with disc herniation) association with greater pain outcome in homozygote patients is P = 0.003, increasing to P = 0.0001 for higher levels of nerve injury (limb amputation). The combined P-value for pain association in all six cohorts tested is 1.14 E-08. The risk profile of this marker is additive: two copies confer the most, one intermediate and none the least risk. Relative degrees of enhanced risk vary between cohorts, but for patients with lumbar back pain, they range between 2- and 3-fold. Although work still remains to define the potential role of this protein in the pathogenic process, here we present the KCNS1 allele rs734784 as one of the first prognostic indicators of chronic pain risk. Screening for this allele could help define those individuals prone to a transition to persistent pain, and thus requiring therapeutic strategies or lifestyle changes that minimize nerve injury. Microarrays were run on mRNA extracted from adult rat L4 and L5 DRGs cells after 3,7,21,40 hours after three different sciatic nerve lesions [Spared Nerve Injury (SNI); Chronic Constriction Injury (CCI); Spinal Nerve Ligation (Ch) with Sham controls (SH)].
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Project description:Chronic pain is a persistent unpleasant sensation that produces pathological synaptic plasticity in the central nervous system. Some of the studies demonstrate that the anterior cingulate cortex (ACC) is a critical area for nociceptive and chronic pain processing. Our previous study revealed that animal models of chronic pain alter excitatory and inhibitory synaptic transmission in the ACC. However, it is not clear what molecules are involved in the alterations of synaptic plasticity in the ACC of chronic pain models. To identify genes with altered expression in the ACC of a chronic pain model, whole transcriptome analysis were performed. In addition to the ACC, whole transcriptome analysis was also performed in the hippocampus, a brain region that has not been reported to be associated with chronic pain. Complete freund's adjuvant (CFA, Sigma-Aldrich, #F5881) into the left hind paw was used for induce chronic inflammatory pain in this study.
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