Abstract
Peripheral nerve injury often causes neuropathic pain and is associated with changes in the expression of numerous proteins in the dorsal horn of the spinal cord. To date, proteomic analysis method has been used to simultaneously analyze hundreds or thousands of proteins differentially expressed in the dorsal horn of the spinal cord in rats or dorsal root ganglion of rats with certain type of peripheral nerve injury. However, a proteomic study using a mouse model of neuropathic pain could be attempted because of abundant protein database and the availability of transgenic mice. In this study, whole proteins were extracted from the ipsilateral dorsal half of the 4th–6th lumbar spinal cord in a mouse model of spared nerve injury (SNI)-induced neuropathic pain. In-gel digests of the proteins size-separated on a polyacrylamide gel were subjected to reverse-phase liquid-chromatography coupled with electrospray ionization ion trap tandem mass spectrometry (MS/MS). After identifying proteins, the data were analyzed with subtractive proteomics usingProtAn, an in-house analytic program. Consequently, 15 downregulated and 35 upregulated proteins were identified in SNI mice. The identified proteins may contribute to the maintenance of neuropathic pain, and may provide new or valuable information in the discovery of new therapeutic targets for neuropathic pain.
Highlights
Various peripheral nerve injuries often result in the development of chronic neuropathic pain, which can be characterized by spontaneous pain, allodynia and hyperalgesia[1]
The central mechanisms relate to hypersensitive responses of spinal dorsal horn (DH) neurons to stimuli; the biochemical molecules that contribute to DH hypersen
The extracted protein sample from each mouse was resolved by SDS-PAGE, and each gel was cut into 15 pieces (Fig. 1C)
Summary
Various peripheral nerve injuries often result in the development of chronic neuropathic pain, which can be characterized by spontaneous pain, allodynia and hyperalgesia[1]. CLC number: R741, Document code: A The authors reported no conflict of interests The persistent activity of, or the release of neurotransmitters and proinflammatory cytokines from the central terminals, of dorsal root ganglion (DRG) neurons drives abnormal gene and protein expression in the spinal DH[1]. These processes support the hypersensitive state of the spinal DH, described as "central sensitization"[2]. Identifying proteins with altered expression in the DH following peripheral nerve damage is essential to elucidate the central mechanisms of neuropathic pain
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