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Arraystar lncRNA and mRNA array data for dorsal root ganglia neurons of mice

ABSTRACT: Nerve injury induces long-lasting pathological pain, namely neuropathic pain (NP), which is dysfunction of the whole pain transmission process, including dorsal root ganglia (DRG) in peripheral nerve system (PNS). Melatonin is well known over a long period of time as hormone of circadian rhythm closely related with the various aspects of pain conditions. Melatonin and melatonin related receptors (MTR1A and MTR1B) exerted amazing analgesic effect in many acute and chronic pain experimental studies, including electrically induced pain, thermally induced pain, mechanical induction of pain and chemical induction of pain. However, the anti-nociceptive action of melatonin in NP is still controversial and unclear. In the present study, our research firstly demonstrated the expression of melatonin receptors in the DRGs, and what more interesting is that MTR1A and MTR1B have a completely different cell type location (MTR1A in the satellite cells and MTR1B in the neurons). In order to get a basic glance at the effects of melatonin and MTR1B on the DRG neurons, a microarray analysis is applied to screen the pain related different expression genes in the primary DRGs cultured neurons with treatment of 1mM melatonin, 100μM MTR1B agonist 8-M-PDOT or vehicle (1% ethanol of normal saline). Subsequent examination was performed, and the finding suggested that melatonin suppressed neuropathic pain via MTR1B dependent and independent pathways in dorsal root ganglia neurons. And MTR1B in DRG may be a potential therapeutic target for NP.

ORGANISM(S): Mus musculus

PROVIDER: GSE89289 | GEO | 2016/11/05

SECONDARY ACCESSION(S): PRJNA352547

REPOSITORIES: GEO

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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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Arraystar lncRNA and mRNA array data for dorsal root ganglia neurons of mice

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