南方科技大学知识苑(SUSTech KC): IFNβ Treatment Inhibits Nerve Injury-induced Mechanical Allodynia and MAPK Signaling By Activating ISG15 in Mouse Spinal Cord

题名	IFNβ Treatment Inhibits Nerve Injury-induced Mechanical Allodynia and MAPK Signaling By Activating ISG15 in Mouse Spinal Cord
作者	Liu，Su 1,2; Karaganis，Stephen 1,3; Mo，Ru Fan1 ; Li，Xiao Xiao 2; Wen，Ruo Xin 1; Song，Xue Jun1
发表日期	2019
DOI	10.1016/j.jpain.2019.11.010
发表期刊	JOURNAL OF PAIN 影响因子和分区
ISSN	1526-5900
EISSN	1528-8447
卷号	21 期号:7-8页码:836-847
摘要	Neuropathic pain is difficult to treat and remains a major clinical challenge worldwide. While the mechanisms which underlie the development of neuropathic pain are incompletely understood, interferon signaling by the immune system is known to play a role. Here, we demonstrate a role for interferon β (IFNβ) in attenuating mechanical allodynia induced by the spared nerve injury in mice. The results show that intrathecal administration of IFNβ (dosages up to 5,000 U) produces significant, transient, and dose-dependent attenuation of mechanical allodynia without observable effects on motor activity or feeding behavior, as is common with IFN administration. This analgesic effect is mediated by the ubiquitin-like protein interferon-stimulated gene 15 (ISG15), which is potently induced within the spinal cord following intrathecal delivery of IFNβ. Both free and conjugated ISG15 are elevated following IFNβ treatment, and this effect is increased in UBP43 mice lacking a key deconjugating enzyme. The IFNβ-mediated analgesia reduces MAPK signaling activation following nerve injury, and this effect requires induction of ISG15. These findings highlight a new role for IFNβ, ISG15, and MAPK signaling in immunomodulation of neuropathic pain and may lead to new therapeutic possibilities. Perspective: Neuropathic pain is frequently intractable in a clinical setting, and new treatment options are needed. Characterizing the antinociceptive potential of IFNβ and the associated downstream signaling pathways in preclinical models may lead to the development of new therapeutic options for debilitating neuropathies.
关键词	Interferon β interferon-stimulated gene 15 MAPK signaling neuropathic pain UBP43 mutation
相关链接	[Scopus记录]
收录类别	SCI
语种	英语
学校署名	第一
资助项目	National Nature Science Foundation of China (NSFC)[81320108012][NSFC 81671086] ; SUSTech Res Fund[Y01416102]
WOS研究方向	Neurosciences & Neurology
WOS类目	Clinical Neurology ; Neurosciences
WOS记录号	WOS:000582483300008
出版者	CHURCHILL LIVINGSTONE
ESI学科分类	NEUROSCIENCE & BEHAVIOR
Scopus记录号	2-s2.0-85076858601
来源库	Scopus
引用统计	被引频次[WOS]：15
成果类型	期刊论文
条目标识符	http://sustech.caswiz.com/handle/2SGJ60CL/65218
专题	南方科技大学南方科技大学医学院_医学神经科学系
作者单位	1.SUSTech Center for Pain Medicine,Medical School,Southern University of Science and Technology,Shenzhen,China 2.Department of Anesthesiology,Xuzhou Medical University,Xuzhou,China 3.Department of Life,Earth and Environmental Sciences,West Texas A&M University,Amarillo,United States
第一作者单位	南方科技大学
第一作者的第一单位	南方科技大学
推荐引用方式 GB/T 7714	Liu，Su,Karaganis，Stephen,Mo，Ru Fan,et al. IFNβ Treatment Inhibits Nerve Injury-induced Mechanical Allodynia and MAPK Signaling By Activating ISG15 in Mouse Spinal Cord[J]. JOURNAL OF PAIN,2019,21(7-8):836-847.
APA	Liu，Su,Karaganis，Stephen,Mo，Ru Fan,Li，Xiao Xiao,Wen，Ruo Xin,&Song，Xue Jun.(2019).IFNβ Treatment Inhibits Nerve Injury-induced Mechanical Allodynia and MAPK Signaling By Activating ISG15 in Mouse Spinal Cord.JOURNAL OF PAIN,21(7-8),836-847.
MLA	Liu，Su,et al."IFNβ Treatment Inhibits Nerve Injury-induced Mechanical Allodynia and MAPK Signaling By Activating ISG15 in Mouse Spinal Cord".JOURNAL OF PAIN 21.7-8(2019):836-847.