An early granulocyte colony-stimulating factor treatment attenuates neuropathic pain through activation of mu opioid receptors on the injured nerve

Ming Feng Liao, Shin Rung Yeh, Ai Lun Lo, Po Kuan Chao, Yun Lin Lee, Yu Hui Hung, Kwok-Tung Lu, Long Sun Ro

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Several studies have shown that the mu opioid receptor (MOR) located in the peripheral nerves can be activated after nerve injury and that it attenuates peripheral nociceptive signals to the spinal dorsal horn. Various cytokines and phosphorylated-p38 (p-p38) activation in the dorsal horn also play an important role in neuropathic pain development. Granulocyte-colony stimulating factor (GCSF) is a growth factor that can stimulate granulocyte formation and has been shown to exert an analgesic effect on neuropathic pain through recruiting opioid-containing leukocytes to the injured nerve. However, the underlying mechanisms are not well understood. Herein, the results of behavior tests in addition to MOR levels in the injured sciatic nerve and the levels of p-p38 and various cytokines in the spinal dorsal horn were studied in vehicle-treated or GCSF-treated chronic constriction injured (CCI) rats at different time points (i.e., 1, 3, and 7 days, respectively) after nerve injury. The results showed that a single early systemic GCSF treatment after nerve injury can up-regulate MORs in the injured nerve, which can decrease peripheral nociceptive signals. Thereafter, those changes suppress the pro-inflammatory cytokine IL-6 but enhance the anti-inflammatory cytokine IL-4, followed by decreases in p-p38 in the dorsal horn, and thus further attenuate neuropathic pain.

Original languageEnglish
Article number25490
JournalScientific Reports
Volume6
DOIs
Publication statusPublished - 2016 May 16

Fingerprint

mu Opioid Receptor
Neuralgia
Granulocyte Colony-Stimulating Factor
Cytokines
Wounds and Injuries
Sciatic Nerve
Therapeutics
Peripheral Nerves
Granulocytes
Constriction
Interleukin-4
Opioid Analgesics
Analgesics
Interleukin-6
Intercellular Signaling Peptides and Proteins
Leukocytes
Anti-Inflammatory Agents
Up-Regulation
Spinal Cord Dorsal Horn

ASJC Scopus subject areas

  • General

Cite this

An early granulocyte colony-stimulating factor treatment attenuates neuropathic pain through activation of mu opioid receptors on the injured nerve. / Liao, Ming Feng; Yeh, Shin Rung; Lo, Ai Lun; Chao, Po Kuan; Lee, Yun Lin; Hung, Yu Hui; Lu, Kwok-Tung; Ro, Long Sun.

In: Scientific Reports, Vol. 6, 25490, 16.05.2016.

Research output: Contribution to journalArticle

Liao, Ming Feng ; Yeh, Shin Rung ; Lo, Ai Lun ; Chao, Po Kuan ; Lee, Yun Lin ; Hung, Yu Hui ; Lu, Kwok-Tung ; Ro, Long Sun. / An early granulocyte colony-stimulating factor treatment attenuates neuropathic pain through activation of mu opioid receptors on the injured nerve. In: Scientific Reports. 2016 ; Vol. 6.
@article{8f0c232ba37e45588fb6bf0ba2014829,
title = "An early granulocyte colony-stimulating factor treatment attenuates neuropathic pain through activation of mu opioid receptors on the injured nerve",
abstract = "Several studies have shown that the mu opioid receptor (MOR) located in the peripheral nerves can be activated after nerve injury and that it attenuates peripheral nociceptive signals to the spinal dorsal horn. Various cytokines and phosphorylated-p38 (p-p38) activation in the dorsal horn also play an important role in neuropathic pain development. Granulocyte-colony stimulating factor (GCSF) is a growth factor that can stimulate granulocyte formation and has been shown to exert an analgesic effect on neuropathic pain through recruiting opioid-containing leukocytes to the injured nerve. However, the underlying mechanisms are not well understood. Herein, the results of behavior tests in addition to MOR levels in the injured sciatic nerve and the levels of p-p38 and various cytokines in the spinal dorsal horn were studied in vehicle-treated or GCSF-treated chronic constriction injured (CCI) rats at different time points (i.e., 1, 3, and 7 days, respectively) after nerve injury. The results showed that a single early systemic GCSF treatment after nerve injury can up-regulate MORs in the injured nerve, which can decrease peripheral nociceptive signals. Thereafter, those changes suppress the pro-inflammatory cytokine IL-6 but enhance the anti-inflammatory cytokine IL-4, followed by decreases in p-p38 in the dorsal horn, and thus further attenuate neuropathic pain.",
author = "Liao, {Ming Feng} and Yeh, {Shin Rung} and Lo, {Ai Lun} and Chao, {Po Kuan} and Lee, {Yun Lin} and Hung, {Yu Hui} and Kwok-Tung Lu and Ro, {Long Sun}",
year = "2016",
month = "5",
day = "16",
doi = "10.1038/srep25490",
language = "English",
volume = "6",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "Nature Publishing Group",

}

TY - JOUR

T1 - An early granulocyte colony-stimulating factor treatment attenuates neuropathic pain through activation of mu opioid receptors on the injured nerve

AU - Liao, Ming Feng

AU - Yeh, Shin Rung

AU - Lo, Ai Lun

AU - Chao, Po Kuan

AU - Lee, Yun Lin

AU - Hung, Yu Hui

AU - Lu, Kwok-Tung

AU - Ro, Long Sun

PY - 2016/5/16

Y1 - 2016/5/16

N2 - Several studies have shown that the mu opioid receptor (MOR) located in the peripheral nerves can be activated after nerve injury and that it attenuates peripheral nociceptive signals to the spinal dorsal horn. Various cytokines and phosphorylated-p38 (p-p38) activation in the dorsal horn also play an important role in neuropathic pain development. Granulocyte-colony stimulating factor (GCSF) is a growth factor that can stimulate granulocyte formation and has been shown to exert an analgesic effect on neuropathic pain through recruiting opioid-containing leukocytes to the injured nerve. However, the underlying mechanisms are not well understood. Herein, the results of behavior tests in addition to MOR levels in the injured sciatic nerve and the levels of p-p38 and various cytokines in the spinal dorsal horn were studied in vehicle-treated or GCSF-treated chronic constriction injured (CCI) rats at different time points (i.e., 1, 3, and 7 days, respectively) after nerve injury. The results showed that a single early systemic GCSF treatment after nerve injury can up-regulate MORs in the injured nerve, which can decrease peripheral nociceptive signals. Thereafter, those changes suppress the pro-inflammatory cytokine IL-6 but enhance the anti-inflammatory cytokine IL-4, followed by decreases in p-p38 in the dorsal horn, and thus further attenuate neuropathic pain.

AB - Several studies have shown that the mu opioid receptor (MOR) located in the peripheral nerves can be activated after nerve injury and that it attenuates peripheral nociceptive signals to the spinal dorsal horn. Various cytokines and phosphorylated-p38 (p-p38) activation in the dorsal horn also play an important role in neuropathic pain development. Granulocyte-colony stimulating factor (GCSF) is a growth factor that can stimulate granulocyte formation and has been shown to exert an analgesic effect on neuropathic pain through recruiting opioid-containing leukocytes to the injured nerve. However, the underlying mechanisms are not well understood. Herein, the results of behavior tests in addition to MOR levels in the injured sciatic nerve and the levels of p-p38 and various cytokines in the spinal dorsal horn were studied in vehicle-treated or GCSF-treated chronic constriction injured (CCI) rats at different time points (i.e., 1, 3, and 7 days, respectively) after nerve injury. The results showed that a single early systemic GCSF treatment after nerve injury can up-regulate MORs in the injured nerve, which can decrease peripheral nociceptive signals. Thereafter, those changes suppress the pro-inflammatory cytokine IL-6 but enhance the anti-inflammatory cytokine IL-4, followed by decreases in p-p38 in the dorsal horn, and thus further attenuate neuropathic pain.

UR - http://www.scopus.com/inward/record.url?scp=84974623555&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84974623555&partnerID=8YFLogxK

U2 - 10.1038/srep25490

DO - 10.1038/srep25490

M3 - Article

C2 - 27180600

AN - SCOPUS:84974623555

VL - 6

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

M1 - 25490

ER -