Role of SIP30 in the development and maintenance of peripheral nerve injury-induced neuropathic pain

Yu Qiu Zhang, Ning Guo, Guangdun Peng, Mei Han, Jeremy Raincrow, Chi hua Chiu, Lique M. Coolen, Robert J. Wenthold, Zhi Qi Zhao, Naihe Jing, Lei Yu

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Using the chronic constriction injury (CCI) model of neuropathic pain, we profiled gene expression in the rat spinal cord, and identified SIP30 as a gene whose expression was elevated after CCI. SIP30 was previously shown to interact with SNAP25, but whose function was otherwise unknown. We now show that in the spinal cord, SIP30 was present in the dorsal horn laminae where the peripheral nociceptive inputs first synapse, co-localizing with nociception-related neuropeptides CGRP and substance P. With the onset of neuropathic pain after CCI surgery, SIP30 mRNA and protein levels increased in the ipsilateral side of the spinal cord, suggesting a potential association between SIP30 and neuropathic pain. When CCI-upregulated SIP30 was inhibited by intrathecal antisense oligonucleotide administration, neuropathic pain was attenuated. This neuropathic pain-reducing effect was observed both during neuropathic pain onset following CCI, and after neuropathic pain was fully established, implicating SIP30 involvement in the development and maintenance phases of neuropathic pain. Using a secretion assay in PC12 cells, anti-SIP30 siRNA decreased the total pool of synaptic vesicles available for exocytosis, pointing to a potential function for SIP30. These results suggest a role of SIP30 in the development and maintenance of peripheral nerve injury-induced neuropathic pain.

Original languageEnglish (US)
Pages (from-to)130-140
Number of pages11
JournalPain
Volume146
Issue number1-2
DOIs
StatePublished - Nov 2009

Fingerprint

Peripheral Nerve Injuries
Neuralgia
Maintenance
Constriction
Wounds and Injuries
Spinal Cord
Gene Expression
Nociception
Synaptic Vesicles
Antisense Oligonucleotides
PC12 Cells
Exocytosis
Substance P
Neuropeptides
Synapses
Small Interfering RNA
Messenger RNA

All Science Journal Classification (ASJC) codes

  • Neurology
  • Clinical Neurology
  • Anesthesiology and Pain Medicine

Keywords

  • Chronic constriction injury
  • Dorsal horn
  • Intrathecal
  • Neuropathic pain
  • SIP30
  • Spinal cord

Cite this

Zhang, Yu Qiu ; Guo, Ning ; Peng, Guangdun ; Han, Mei ; Raincrow, Jeremy ; Chiu, Chi hua ; Coolen, Lique M. ; Wenthold, Robert J. ; Zhao, Zhi Qi ; Jing, Naihe ; Yu, Lei. / Role of SIP30 in the development and maintenance of peripheral nerve injury-induced neuropathic pain. In: Pain. 2009 ; Vol. 146, No. 1-2. pp. 130-140.
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Zhang, YQ, Guo, N, Peng, G, Han, M, Raincrow, J, Chiu, CH, Coolen, LM, Wenthold, RJ, Zhao, ZQ, Jing, N & Yu, L 2009, 'Role of SIP30 in the development and maintenance of peripheral nerve injury-induced neuropathic pain', Pain, vol. 146, no. 1-2, pp. 130-140. https://doi.org/10.1016/j.pain.2009.07.011

Role of SIP30 in the development and maintenance of peripheral nerve injury-induced neuropathic pain. / Zhang, Yu Qiu; Guo, Ning; Peng, Guangdun; Han, Mei; Raincrow, Jeremy; Chiu, Chi hua; Coolen, Lique M.; Wenthold, Robert J.; Zhao, Zhi Qi; Jing, Naihe; Yu, Lei.

In: Pain, Vol. 146, No. 1-2, 11.2009, p. 130-140.

Research output: Contribution to journalArticle

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T1 - Role of SIP30 in the development and maintenance of peripheral nerve injury-induced neuropathic pain

AU - Zhang, Yu Qiu

AU - Guo, Ning

AU - Peng, Guangdun

AU - Han, Mei

AU - Raincrow, Jeremy

AU - Chiu, Chi hua

AU - Coolen, Lique M.

AU - Wenthold, Robert J.

AU - Zhao, Zhi Qi

AU - Jing, Naihe

AU - Yu, Lei

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N2 - Using the chronic constriction injury (CCI) model of neuropathic pain, we profiled gene expression in the rat spinal cord, and identified SIP30 as a gene whose expression was elevated after CCI. SIP30 was previously shown to interact with SNAP25, but whose function was otherwise unknown. We now show that in the spinal cord, SIP30 was present in the dorsal horn laminae where the peripheral nociceptive inputs first synapse, co-localizing with nociception-related neuropeptides CGRP and substance P. With the onset of neuropathic pain after CCI surgery, SIP30 mRNA and protein levels increased in the ipsilateral side of the spinal cord, suggesting a potential association between SIP30 and neuropathic pain. When CCI-upregulated SIP30 was inhibited by intrathecal antisense oligonucleotide administration, neuropathic pain was attenuated. This neuropathic pain-reducing effect was observed both during neuropathic pain onset following CCI, and after neuropathic pain was fully established, implicating SIP30 involvement in the development and maintenance phases of neuropathic pain. Using a secretion assay in PC12 cells, anti-SIP30 siRNA decreased the total pool of synaptic vesicles available for exocytosis, pointing to a potential function for SIP30. These results suggest a role of SIP30 in the development and maintenance of peripheral nerve injury-induced neuropathic pain.

AB - Using the chronic constriction injury (CCI) model of neuropathic pain, we profiled gene expression in the rat spinal cord, and identified SIP30 as a gene whose expression was elevated after CCI. SIP30 was previously shown to interact with SNAP25, but whose function was otherwise unknown. We now show that in the spinal cord, SIP30 was present in the dorsal horn laminae where the peripheral nociceptive inputs first synapse, co-localizing with nociception-related neuropeptides CGRP and substance P. With the onset of neuropathic pain after CCI surgery, SIP30 mRNA and protein levels increased in the ipsilateral side of the spinal cord, suggesting a potential association between SIP30 and neuropathic pain. When CCI-upregulated SIP30 was inhibited by intrathecal antisense oligonucleotide administration, neuropathic pain was attenuated. This neuropathic pain-reducing effect was observed both during neuropathic pain onset following CCI, and after neuropathic pain was fully established, implicating SIP30 involvement in the development and maintenance phases of neuropathic pain. Using a secretion assay in PC12 cells, anti-SIP30 siRNA decreased the total pool of synaptic vesicles available for exocytosis, pointing to a potential function for SIP30. These results suggest a role of SIP30 in the development and maintenance of peripheral nerve injury-induced neuropathic pain.

KW - Chronic constriction injury

KW - Dorsal horn

KW - Intrathecal

KW - Neuropathic pain

KW - SIP30

KW - Spinal cord

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