Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0423716 (Neuropathic pain)
 1,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Objective: To explore the potential regulation mechanisms of miR-384-5p in Neuropathic pain (NP).Methods: Rat model of chronic constriction injury (CCI) was established to induce NP in vivo. NP levels were assessed using Withdrawal Threshold (PWT) and Paw Withdrawal Latency (PWL). qPCR and Western blotting were used to determine the relative expression of miR-384-5p and SCN3A. The inflammation response in spinal microglia cells was determined by ELISA assay. Immunofluorescence assay was used to demonstrate the co-localization of miR-384-5p with SCN3A in rat dorsal root ganglions (DRGs). The target genes of miR-384-5p were verified by dual-luciferase report assays.Results: In the current study, the miR-384-5p expression level was significantly downregulated in CCI rats when comparing to the sham group. In addition, miR-384-5p agomir significantly repressed mechanical allodynia and heat hyperalgesia in CCI rats. Meanwhile, the current study indicated miR-384-5p could decrease inflammation progress in spinal microglia cells incubated in lipopolysaccharide. Consistently, overexpression of miR-384-5p obviously depressed inflammation cytokine levels in CCI rats. Dual-luciferase reporter assays indicated that SCN3A is a target gene of miR-384-5p.Conclusion: miR-384-5p is a negative regulator in the development of neuropathic pain by regulating SCN3A, indicating that miR-384-5p might be a promising therapeutic target in the treatment of neuropathic pain.Abbreviations: CCI: Chronic constriction injury; ZEB1: Zinc finger E box binding protein-1; MAPK6: Mitogen-activated protein kinase 6; COX-2: cyclooxygenase-2.
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PMID:miR-384-5p ameliorates neuropathic pain by targeting SCN3A in a rat model of chronic constriction injury. 3209 88

Neuropathic pain is defined as a chronic pain. It could be resulted from a lesion of nervous systems. MicroRNAs have been reported to modulate multiple genes and pathways in neuropathic pain and neuroinflammation. Therefore, identifying the potential expression patterns of microRNAs under neuropathic pain conditions is significant. miR-128-3p has been identified in many cancers. But, its biological role in neuropathic pain progression remains poorly known. Currently, we aimed to explore the possible functions of miR-128-3p in the modulation of neuropathic pain. We displayed in the CCI rats, miR-128-3p was greatly down-regulated in the spinal cord tissues and the isolated microglias. Subsequently, LV-miR-128-3p could attenuate CCI-triggered mechanical allodynia and thermal hyperalgesia. Meanwhile, some common pro-inflammatory cytokines were significantly reduced while anti-inflammatory cytokine IL-10 was increased by miR-128-3p. Here, in the current investigation, by utilizing dual-luciferase reporter assays, ZEB1 was proved as a direct target of miR-128-3p. LV-miR-128-3p significantly repressed ZEB1 expression in microglia of CCI rats. Moreover, ZEB1 was reported to be increased in CCI rats. miR-128-3p rescued the effects of ZEB1 on neuropathic pain progression via inhibiting neuroinflammation. Taken these together, we implied miR-128-3p alleviated the progression of neuropathic pain via modulating ZEB1.
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PMID:MicroRNA-128-3p Alleviates Neuropathic Pain Through Targeting ZEB1. 3227 27