Abstract
PurposeThis aim of this study was to investigate the key genes and pathways involved in the response to pain in goat and sheep by transcriptome sequencing.MethodsChronic pain was induced with the injection of the complete Freund’s adjuvant (CFA) in sheep and goats. The animals were divided into four groups: CFA-treated sheep, control sheep, CFA-treated goat, and control goat groups (n = 3 in each group). The dorsal root ganglions of these animals were isolated and used for the construction of a cDNA library and transcriptome sequencing. Differentially expressed genes (DEGs) were identified in CFA-induced sheep and goats and gene ontology (GO) enrichment analysis was performed.ResultsIn total, 1748 and 2441 DEGs were identified in CFA-treated goat and sheep, respectively. The DEGs identified in CFA-treated goats, such as C-C motif chemokine ligand 27 (CCL27), glutamate receptor 2 (GRIA2), and sodium voltage-gated channel alpha subunit 3 (SCN3A), were mainly enriched in GO functions associated with N-methyl-d-aspartate (NMDA) receptor, inflammatory response, and immune response. The DEGs identified in CFA-treated sheep, such as gamma-aminobutyric acid (GABA)-related DEGs (gamma-aminobutyric acid type A receptor gamma 3 subunit [GABRG3], GABRB2, and GABRB1), SCN9A, and transient receptor potential cation channel subfamily V member 1 (TRPV1), were mainly enriched in GO functions related to neuroactive ligand-receptor interaction, NMDA receptor, and defense response.ConclusionsOur data indicate that NMDA receptor, inflammatory response, and immune response as well as key DEGs such as CCL27, GRIA2, and SCN3A may regulate the process of pain response during chronic pain in goats. Neuroactive ligand-receptor interaction and NMDA receptor as well as GABA-related DEGs, SCN9A, and TRPV1 may modulate the process of response to pain in sheep. These DEGs may serve as drug targets for preventing chronic pain.
Highlights
Chronic pain is considered as a major physical and mental health problem
This dose was chosen for the following reasons: After the injection of 1 mL of complete Freund’s adjuvant (CFA), pain responses such as redness, swelling, and hyperalgesia were markedly observed at the injection site in both sheep and goats, indicating that the inflammatory pain was successfully induced by CFA; the induction effect was not satisfactory under or above this dose of CFA
We found that the differentially expressed gene (DEG) only identified in goat, such as immunoglobulin superfamily member 6 (IGSF6), C-X-C motif chemokine ligand 11 (CXCL11), pentraxin 3 (PTX3), C-C motif chemokine ligand 17 (CCL17), and chemokine (C-C motif ) receptor-like 1 (CCRL1) were significantly enriched in chemokine signaling pathway, chemotaxis, inflammatory response, cytokine–cytokine receptor interaction, and immune response (Additional file 1: Table S2), while the DEGs only identified in sheep, including colony-stimulating factor 2 (CSF2), CCAAT/ enhancer binding protein gamma (CEBPG), RELB proto-oncogene, nuclear factor kappa B (NF-KB) subunit (RELB), B cell CLL/lymphoma 3 (BCL3), and integrin subunit beta 1 (ITGB1), were markedly enriched in intermediate filament, leukocyte differentiation, B cell activation, cellular response to stress, cytokine–cytokine receptor interaction, and cell–cell signaling (Additional file 1: Table S2)
Summary
Chronic pain is considered as a major physical and mental health problem. Millions of people are affected by uncomfortable conditions such as back pain, headache, and arthritis [1, 2]. The differential expression of ATP-gated P2X receptors in DRG is shown to play important roles in the regulation of nociceptive mechanisms in chronic neuropathic pain and visceralgia rat models [14]. The transient receptor potential melastatin 8 in DRG plays a key role in chronic neuropathic pain [15]. Microarray analysis of DRG gene expression has been used for the identification of key cytokines involved in the regulation of chronic pain [16]. Despite these advances, the regulatory mechanisms mediating the development of chronic pain are largely unknown. Given that the spinal DRG is the primary center for the conduction and maintenance of pain, studies on DRG transcriptome may be helpful for the comprehensive and systematic elucidation of the key regulatory mechanisms underlying chronic pain
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