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A nerve injury–specific long noncoding RNA promotes neuropathic pain by increasing Ccl2 expression
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A nerve injury–specific long noncoding RNA promotes neuropathic pain by increasing Ccl2 expression
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Journal Article
A nerve injury–specific long noncoding RNA promotes neuropathic pain by increasing Ccl2 expression
2022
Overview
Maladaptive changes of nerve injury-associated genes in dorsal root ganglia (DRGs) are critical for neuropathic pain genesis. Emerging evidence supports the role of long noncoding RNAs (lncRNAs) in regulating gene transcription. Here we identified a conserved lncRNA, named nerve injury-specific lncRNA (NIS-lncRNA) for its upregulation in injured DRGs exclusively in response to nerve injury. This upregulation was triggered by nerve injury-induced increase in DRG ELF1, a transcription factor that bound to the NIS-lncRNA promoter. Blocking this upregulation attenuated nerve injury-induced CCL2 increase in injured DRGs and nociceptive hypersensitivity during the development and maintenance periods of neuropathic pain. Mimicking NIS-lncRNA upregulation elevated CCL2 expression, increased CCL2-mediated excitability in DRG neurons, and produced neuropathic pain symptoms. Mechanistically, NIS-lncRNA recruited more binding of the RNA-interacting protein FUS to the Ccl2 promoter and augmented Ccl2 transcription in injured DRGs. Thus, NIS-lncRNA participates in neuropathic pain likely by promoting FUS-triggered DRG Ccl2 expression and may be a potential target in neuropathic pain management.
Publisher
American Society for Clinical Investigation
Subject
/ Complications and side effects
/ Ganglia, Spinal - metabolism
/ Humans
/ Monocyte chemoattractant protein 1
/ Peripheral Nerve Injuries - genetics
/ Peripheral Nerve Injuries - metabolism
/ Peripheral Nerve Injuries - pathology
/ Proteins
/ RNA
/ RNA, Long Noncoding - genetics
/ RNA, Long Noncoding - metabolism
/ Surgery
