The c-kit signaling pathway is involved in the development of persistent pain

Yan Gang Sun, Neilia G. Gracias, Julie Kosto Drobish, Michael Vasko, Robert W. Gereau, Zhou Feng Chen

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Protein kinase signal transduction pathways play critical roles in regulating nociception. Here we show that c-kit, a tyrosine kinase receptor, is expressed in lamina I and II layer of the dorsal horn. Moreover, the superficial c-kit+ fibers originate from the dorsal root ganglion, and c-kit in lamina II inner layer comes from intrinsic expression of the spinal cord. KitW-v mice, which contain a hypomorphic mutation, exhibited normal acute pain in most pain behavior tests. In the formalin test, the first phase was not affected, whereas the second phase pain response of KitW-v mice was significantly reduced relative to wild-type littermates. KitW-v mice also showed abnormal neuropathic pain, notably in the contralateral side of nerve injury. The expression and release of CGRP and substance P were not altered by the c-kit mutation. Together, these results implicate c-kit-mediated signal transduction in the development of persistent pain.

Original languageEnglish
Pages (from-to)178-186
Number of pages9
JournalPain
Volume144
Issue number1-2
DOIs
StatePublished - Jul 2009

Fingerprint

Substantia Gelatinosa
Pain
Signal Transduction
Mutation
Nociception
Acute Pain
Spinal Ganglia
Receptor Protein-Tyrosine Kinases
Neuralgia
Pain Measurement
Substance P
Protein Kinases
Spinal Cord
Wounds and Injuries
Spinal Cord Dorsal Horn

Keywords

  • c-kit
  • CCI
  • DRG
  • Formalin test
  • Persistent pain
  • Spinal cord
  • Tyrosine kinase receptor

ASJC Scopus subject areas

  • Clinical Neurology
  • Anesthesiology and Pain Medicine
  • Neurology
  • Pharmacology

Cite this

Sun, Y. G., Gracias, N. G., Drobish, J. K., Vasko, M., Gereau, R. W., & Chen, Z. F. (2009). The c-kit signaling pathway is involved in the development of persistent pain. Pain, 144(1-2), 178-186. https://doi.org/10.1016/j.pain.2009.04.011

The c-kit signaling pathway is involved in the development of persistent pain. / Sun, Yan Gang; Gracias, Neilia G.; Drobish, Julie Kosto; Vasko, Michael; Gereau, Robert W.; Chen, Zhou Feng.

In: Pain, Vol. 144, No. 1-2, 07.2009, p. 178-186.

Research output: Contribution to journalArticle

Sun, YG, Gracias, NG, Drobish, JK, Vasko, M, Gereau, RW & Chen, ZF 2009, 'The c-kit signaling pathway is involved in the development of persistent pain', Pain, vol. 144, no. 1-2, pp. 178-186. https://doi.org/10.1016/j.pain.2009.04.011
Sun, Yan Gang ; Gracias, Neilia G. ; Drobish, Julie Kosto ; Vasko, Michael ; Gereau, Robert W. ; Chen, Zhou Feng. / The c-kit signaling pathway is involved in the development of persistent pain. In: Pain. 2009 ; Vol. 144, No. 1-2. pp. 178-186.
@article{0a586da037d04034bee46a8fa4647e13,
title = "The c-kit signaling pathway is involved in the development of persistent pain",
abstract = "Protein kinase signal transduction pathways play critical roles in regulating nociception. Here we show that c-kit, a tyrosine kinase receptor, is expressed in lamina I and II layer of the dorsal horn. Moreover, the superficial c-kit+ fibers originate from the dorsal root ganglion, and c-kit in lamina II inner layer comes from intrinsic expression of the spinal cord. KitW-v mice, which contain a hypomorphic mutation, exhibited normal acute pain in most pain behavior tests. In the formalin test, the first phase was not affected, whereas the second phase pain response of KitW-v mice was significantly reduced relative to wild-type littermates. KitW-v mice also showed abnormal neuropathic pain, notably in the contralateral side of nerve injury. The expression and release of CGRP and substance P were not altered by the c-kit mutation. Together, these results implicate c-kit-mediated signal transduction in the development of persistent pain.",
keywords = "c-kit, CCI, DRG, Formalin test, Persistent pain, Spinal cord, Tyrosine kinase receptor",
author = "Sun, {Yan Gang} and Gracias, {Neilia G.} and Drobish, {Julie Kosto} and Michael Vasko and Gereau, {Robert W.} and Chen, {Zhou Feng}",
year = "2009",
month = "7",
doi = "10.1016/j.pain.2009.04.011",
language = "English",
volume = "144",
pages = "178--186",
journal = "Pain",
issn = "0304-3959",
publisher = "Elsevier",
number = "1-2",

}

TY - JOUR

T1 - The c-kit signaling pathway is involved in the development of persistent pain

AU - Sun, Yan Gang

AU - Gracias, Neilia G.

AU - Drobish, Julie Kosto

AU - Vasko, Michael

AU - Gereau, Robert W.

AU - Chen, Zhou Feng

PY - 2009/7

Y1 - 2009/7

N2 - Protein kinase signal transduction pathways play critical roles in regulating nociception. Here we show that c-kit, a tyrosine kinase receptor, is expressed in lamina I and II layer of the dorsal horn. Moreover, the superficial c-kit+ fibers originate from the dorsal root ganglion, and c-kit in lamina II inner layer comes from intrinsic expression of the spinal cord. KitW-v mice, which contain a hypomorphic mutation, exhibited normal acute pain in most pain behavior tests. In the formalin test, the first phase was not affected, whereas the second phase pain response of KitW-v mice was significantly reduced relative to wild-type littermates. KitW-v mice also showed abnormal neuropathic pain, notably in the contralateral side of nerve injury. The expression and release of CGRP and substance P were not altered by the c-kit mutation. Together, these results implicate c-kit-mediated signal transduction in the development of persistent pain.

AB - Protein kinase signal transduction pathways play critical roles in regulating nociception. Here we show that c-kit, a tyrosine kinase receptor, is expressed in lamina I and II layer of the dorsal horn. Moreover, the superficial c-kit+ fibers originate from the dorsal root ganglion, and c-kit in lamina II inner layer comes from intrinsic expression of the spinal cord. KitW-v mice, which contain a hypomorphic mutation, exhibited normal acute pain in most pain behavior tests. In the formalin test, the first phase was not affected, whereas the second phase pain response of KitW-v mice was significantly reduced relative to wild-type littermates. KitW-v mice also showed abnormal neuropathic pain, notably in the contralateral side of nerve injury. The expression and release of CGRP and substance P were not altered by the c-kit mutation. Together, these results implicate c-kit-mediated signal transduction in the development of persistent pain.

KW - c-kit

KW - CCI

KW - DRG

KW - Formalin test

KW - Persistent pain

KW - Spinal cord

KW - Tyrosine kinase receptor

UR - http://www.scopus.com/inward/record.url?scp=66049094709&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=66049094709&partnerID=8YFLogxK

U2 - 10.1016/j.pain.2009.04.011

DO - 10.1016/j.pain.2009.04.011

M3 - Article

C2 - 19443120

AN - SCOPUS:66049094709

VL - 144

SP - 178

EP - 186

JO - Pain

JF - Pain

SN - 0304-3959

IS - 1-2

ER -