G2A as a Threshold Regulator of Inflammatory Hyperalgesia Modulates Chronic Hyperalgesia

Yeu Shiuan Su; Yu Fen Huang; Jen Wong; Chia Wei Lee; Wei Shan Hsieh; Wei Hsin Sun

doi:10.1007/s12031-017-1000-3

G2A as a Threshold Regulator of Inflammatory Hyperalgesia Modulates Chronic Hyperalgesia

Yeu Shiuan Su, Yu Fen Huang, Jen Wong, Chia Wei Lee, Wei Shan Hsieh, Wei Hsin Sun^*

^*Corresponding author for this work

Department of Life Sciences and Institute of Genome Sciences

Research output: Contribution to journal › Article › peer-review

5 Scopus citations

Abstract

Tissue injury, pathogen infection, and diseases are often accompanied by inflammation to release mediators that sensitize nociceptors and further recruit immune cells, which can lead to chronic hyperalgesia and inflammation. Tissue acidosis, occurring at the inflammatory site, is a major factor contributing to pain and hyperalgesia. The receptor G2 accumulation (G2A), expressed in neurons and immune cells, responds to protons or oxidized free fatty acids such as 9-hydroxyoctadecadienoic acid produced by injured cells or oxidative stresses. We previously found increased G2A expression in mouse dorsal root ganglia (DRG) at 90 min after complete Freund’s adjuvant (CFA)-induced inflammatory pain, but whether G2A is involved in the inflammation or hyperalgesia remained unclear. In this study, we overexpressed or knocked-down G2A gene expression in DRG to explore the roles of G2A. G2A overexpression reduced the infiltration of acute immune cells (granulocytes) and attenuated hyperalgesia at 90 to 240 min after CFA injection. G2A knockdown increased the number of immune cells before CFA injection and prolonged the inflammatory hyperalgesia after CFA injection. G2A may serve as a threshold regulator in neurons to attenuate the initial nociceptive and inflammatory signals, modulating the chronic state of hyperalgesia.

Original language	English
Pages (from-to)	39-50
Number of pages	12
Journal	Journal of Molecular Neuroscience
Volume	64
Issue number	1
DOIs	https://doi.org/10.1007/s12031-017-1000-3
State	Published - 1 Jan 2018

Keywords

G-protein signaling
G2A
GPCRs
Granulocytes
Hyperalgesia
Inflammation

Access to Document

10.1007/s12031-017-1000-3

Cite this

@article{3446842ac3354e909e41106273f17eb1,

title = "G2A as a Threshold Regulator of Inflammatory Hyperalgesia Modulates Chronic Hyperalgesia",

abstract = "Tissue injury, pathogen infection, and diseases are often accompanied by inflammation to release mediators that sensitize nociceptors and further recruit immune cells, which can lead to chronic hyperalgesia and inflammation. Tissue acidosis, occurring at the inflammatory site, is a major factor contributing to pain and hyperalgesia. The receptor G2 accumulation (G2A), expressed in neurons and immune cells, responds to protons or oxidized free fatty acids such as 9-hydroxyoctadecadienoic acid produced by injured cells or oxidative stresses. We previously found increased G2A expression in mouse dorsal root ganglia (DRG) at 90 min after complete Freund{\textquoteright}s adjuvant (CFA)-induced inflammatory pain, but whether G2A is involved in the inflammation or hyperalgesia remained unclear. In this study, we overexpressed or knocked-down G2A gene expression in DRG to explore the roles of G2A. G2A overexpression reduced the infiltration of acute immune cells (granulocytes) and attenuated hyperalgesia at 90 to 240 min after CFA injection. G2A knockdown increased the number of immune cells before CFA injection and prolonged the inflammatory hyperalgesia after CFA injection. G2A may serve as a threshold regulator in neurons to attenuate the initial nociceptive and inflammatory signals, modulating the chronic state of hyperalgesia.",

keywords = "G-protein signaling, G2A, GPCRs, Granulocytes, Hyperalgesia, Inflammation",

author = "Su, {Yeu Shiuan} and Huang, {Yu Fen} and Jen Wong and Lee, {Chia Wei} and Hsieh, {Wei Shan} and Sun, {Wei Hsin}",

note = "Publisher Copyright: {\textcopyright} 2017, Springer Science+Business Media, LLC, part of Springer Nature.",

year = "2018",

month = jan,

day = "1",

doi = "10.1007/s12031-017-1000-3",

language = "English",

volume = "64",

pages = "39--50",

journal = "Journal of Molecular Neuroscience",

issn = "0895-8696",

publisher = "Humana Press",

number = "1",

}

TY - JOUR

T1 - G2A as a Threshold Regulator of Inflammatory Hyperalgesia Modulates Chronic Hyperalgesia

AU - Su, Yeu Shiuan

AU - Huang, Yu Fen

AU - Wong, Jen

AU - Lee, Chia Wei

AU - Hsieh, Wei Shan

AU - Sun, Wei Hsin

PY - 2018/1/1

Y1 - 2018/1/1

N2 - Tissue injury, pathogen infection, and diseases are often accompanied by inflammation to release mediators that sensitize nociceptors and further recruit immune cells, which can lead to chronic hyperalgesia and inflammation. Tissue acidosis, occurring at the inflammatory site, is a major factor contributing to pain and hyperalgesia. The receptor G2 accumulation (G2A), expressed in neurons and immune cells, responds to protons or oxidized free fatty acids such as 9-hydroxyoctadecadienoic acid produced by injured cells or oxidative stresses. We previously found increased G2A expression in mouse dorsal root ganglia (DRG) at 90 min after complete Freund’s adjuvant (CFA)-induced inflammatory pain, but whether G2A is involved in the inflammation or hyperalgesia remained unclear. In this study, we overexpressed or knocked-down G2A gene expression in DRG to explore the roles of G2A. G2A overexpression reduced the infiltration of acute immune cells (granulocytes) and attenuated hyperalgesia at 90 to 240 min after CFA injection. G2A knockdown increased the number of immune cells before CFA injection and prolonged the inflammatory hyperalgesia after CFA injection. G2A may serve as a threshold regulator in neurons to attenuate the initial nociceptive and inflammatory signals, modulating the chronic state of hyperalgesia.

AB - Tissue injury, pathogen infection, and diseases are often accompanied by inflammation to release mediators that sensitize nociceptors and further recruit immune cells, which can lead to chronic hyperalgesia and inflammation. Tissue acidosis, occurring at the inflammatory site, is a major factor contributing to pain and hyperalgesia. The receptor G2 accumulation (G2A), expressed in neurons and immune cells, responds to protons or oxidized free fatty acids such as 9-hydroxyoctadecadienoic acid produced by injured cells or oxidative stresses. We previously found increased G2A expression in mouse dorsal root ganglia (DRG) at 90 min after complete Freund’s adjuvant (CFA)-induced inflammatory pain, but whether G2A is involved in the inflammation or hyperalgesia remained unclear. In this study, we overexpressed or knocked-down G2A gene expression in DRG to explore the roles of G2A. G2A overexpression reduced the infiltration of acute immune cells (granulocytes) and attenuated hyperalgesia at 90 to 240 min after CFA injection. G2A knockdown increased the number of immune cells before CFA injection and prolonged the inflammatory hyperalgesia after CFA injection. G2A may serve as a threshold regulator in neurons to attenuate the initial nociceptive and inflammatory signals, modulating the chronic state of hyperalgesia.

KW - G-protein signaling

KW - G2A

KW - GPCRs

KW - Granulocytes

KW - Hyperalgesia

KW - Inflammation

UR - http://www.scopus.com/inward/record.url?scp=85034602805&partnerID=8YFLogxK

U2 - 10.1007/s12031-017-1000-3

DO - 10.1007/s12031-017-1000-3

M3 - Article

C2 - 29159784

AN - SCOPUS:85034602805

SN - 0895-8696

VL - 64

SP - 39

EP - 50

JO - Journal of Molecular Neuroscience

JF - Journal of Molecular Neuroscience

IS - 1

ER -

G2A as a Threshold Regulator of Inflammatory Hyperalgesia Modulates Chronic Hyperalgesia

Abstract

Keywords

Access to Document

Other files and links

Fingerprint

Cite this