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Neurochem Int. 2014 Nov;77:58-67. doi: 10.1016/j.neuint.2014.05.010. Epub 2014 Jun 3.

Emerging roles of microRNAs in chronic pain.

Author information

1
Department of Pharmacology, Graduate School of Medicine, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan. Electronic address: sa19@nms.ac.jp.
2
Department of Pharmacology, Graduate School of Medicine, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan. Electronic address: hsuzuki@nms.ac.jp.

Abstract

Chronic pain is a debilitating syndrome caused by a variety of disorders, and represents a major clinical problem because of the lack of adequate medication. In chronic pain, massive changes in gene expression are observed in a variety of cells, including neurons and glia, in the overall somatosensory system from the sensory ganglia to the higher central nervous system. The protein expressions of hundreds of genes are thought to be post-transcriptionally regulated by a single type of microRNA in a sequence-specific manner. Recently, critical roles of microRNAs in the pathophysiology of chronic pain have been emerging. Genome-wide screenings of microRNA expression changes have been reported in a variety of painful conditions, including peripheral nerve injury, inflammatory diseases, cancer and spinal cord injury. The data obtained suggest that a wide range of microRNAs change their expressions in individual pain conditions, although the pathological significance of individual microRNAs as causal mediators in distinct pain conditions remains to be revealed for a limited number of microRNAs. Insights into the roles of microRNAs in chronic pain will enhance our understanding of the pathophysiology of chronic pain and allow prompt therapeutic application of microRNA-related drugs against intractable persistent pain.

KEYWORDS:

Astrocyte; Cancer pain; Hyperexcitability; Inflammatory pain; Microglia; Neuroinflammation; Neuropathic pain; Primary sensory neuron; Spinal cord; microRNA

PMID:
24905749
DOI:
10.1016/j.neuint.2014.05.010
[Indexed for MEDLINE]

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