Neuropathic pain is a refractory pain syndrome resulting from lesions or dysfunction of the somatosensory nervous system. Schwann cells, the glial cells of the peripheral nervous system, have been shown to contribute to neuropathic pain through the release of inflammatory mediators. However, the molecular mechanisms that regulate the expression of inflammatory genes in Schwann cells are poorly understood. Long non-coding RNAs (lncRNAs) play a key role in regulating a variety of gene expression processes. Among them, the lncRNA H19 is upregulated in Schwann cells following nerve injury and contributes to neuropathic pain. Therefore, this study aimed to elucidate the function of H19 in Schwann cells. In the rat Schwann cell line, H19 induced the expression of chemokine C-X-C motif chemokine ligand 1 (CXCL1). Consistent with these findings, both H19 and CXCL1 expression were persistently elevated in the injured spinal nerves of rats with neuropathic pain. These findings suggest that H19 upregulation in Schwann cells may contribute to neuropathic pain through the induction of CXCL1 expression.
Miki et al. (Mon,) studied this question.