Spinal IL-36γ/IL-36R participates in the maintenance of chronic inflammatory pain through astroglial JNK pathway-Reference-Cited by-同舟云学术

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Spinal IL-36γ/IL-36R participates in the maintenance of chronic inflammatory pain through astroglial JNK pathway

Published:2018-12-21 Issue:3 Volume:67 Page:438-451
ISSN:0894-1491
Container-title:Glia
language:en
Short-container-title:Glia

Author:

Li Qian¹,Liu Shenbin²,Li Lingling¹,Ji Xiaoli¹,Wang Min¹,Zhou Junmei¹^ORCID

Affiliation:

1. Department of Central Laboratory; Shanghai Children's Hospital, Shanghai Jiaotong University; Shanghai China

2. Department of Integrative Medicine and Neurobiology, State Key Laboratory of Medical Neurobiology; School of Basic Medical Science, Institutes of Brain Science, Collaborative Innovation Center for Brain Science, Fudan Institutes of Integrative Medicine, Fudan University; Shanghai China

Funder

National Natural Science Foundation of China

Foundation of Shanghai Municipal Commission of Health and Family Planning

Shanghai Jiaotong University

China Postdoctoral Science Foundation

Foundation of Shanghai Children's Hospital for Outstanding Young Scientists

Publisher

Wiley

Subject

Cellular and Molecular Neuroscience,Neurology

Link

http://onlinelibrary.wiley.com/wol1/doi/10.1002/glia.23552/fullpdf

Reference50 articles.

1. Imiquimod treatment causes systemic disease in mice resembling generalized Pustular psoriasis in an IL-1 and IL-36 dependent manner;Alvarez;Mediators of Inflammation,2016

2. Regulation of expression of the novel IL-1 receptor family members in the mouse brain;Andre;Journal of Neurochemistry,2005

3. Interleukin (IL) 36 gamma induces mucin 5AC, oligomeric mucus/gel-forming expression via IL-36 receptor-extracellular signal regulated kinase 1 and 2, and p38-nuclear factor kappa-light-chain-enhancer of activated B cells in human airway epithelial cells;Bae;American Journal of Rhinology & Allergy,2018

4. Spinal release of tumour necrosis factor activates c-Jun N-terminal kinase and mediates inflammation-induced hypersensitivity;Bas;European Journal of Pain,2015

5. IL-1Rrp2 expression and IL-1F9 (IL-1H1) actions in brain cells;Berglöf;Journal of Neuroimmunology,2003

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