Selective repression of gene expression in neuropathic pain by the neuron-restrictive silencing factor/repressor element-1 silencing transcription (NRSF/REST)

• Published in: Neuroscience letters 2016-06, Vol.625, p.20-25
• Main Authors: Willis, Dianna E., Wang, Meng, Brown, Elizabeth, Fones, Lilah, Cave, John W.
• Format: Article
• Language: English
• Subjects: Animals; Epigenesis, Genetic; Epigenetics; Gene Expression Regulation; Humans; MeCP2; Neuralgia - genetics; Neuropathic pain; NRSF/REST; Repressor Proteins - genetics
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2015.12.003

•Nerve injury or disease can cause persistent nociceptive hypersensitivity.•Transition is accompanied by changes in the transcriptome of PNS and CNS circuits.•Neuropathic pain is associated with increased NRSF expression.•NRSF represses a subset of its developmental targets after injury. Neuropathic pain often develops following nerve injury as a result of maladaptive changes that occur in the injured nerve and along the nociceptive pathways of the peripheral and central nervous systems. Multiple cellular and molecular mechanisms likely account for these changes; however, the exact nature of these mechanisms remain largely unknown. A growing number of studies suggest that alteration in gene expression is an important step in the progression from acute to chronic pain states and epigenetic regulation has been proposed to drive this change in gene expression. In this review, we discuss recent evidence that the DNA-binding protein neuron-restrictive silencing factor/repressor element-1 silencing transcription factor (NRSF/REST) is an important component in the development and maintenance of neuropathic pain through its role as a transcriptional regulator for a select subset of genes that it normally represses during development.