Bourgoin SG, Hui W. Role of mitogen- and stress-activated kinases in inflammatory arthritis. World J Pharmacol 2015; 4(4): 265-273 [DOI: 10.5497/wjp.v4.i4.265]
Corresponding Author of This Article
Sylvain G Bourgoin, PhD, Division of Infectious Disease and Immunity, CHU de Québec Research Center and Department of Microbiology-Infectious Disease and Immunology, Faculty of Medicine, Laval University, 2705 Boul Laurier, Québec G1V 4G2, Canada. sylvain.bourgoin@crchudequebec.ulaval.ca
Research Domain of This Article
Rheumatology
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Pharmacol. Dec 9, 2015; 4(4): 265-273 Published online Dec 9, 2015. doi: 10.5497/wjp.v4.i4.265
Role of mitogen- and stress-activated kinases in inflammatory arthritis
Sylvain G Bourgoin, Weili Hui
Sylvain G Bourgoin, Weili Hui, Division of Infectious Disease and Immunity, CHU de Québec Research Center and Department of Microbiology-Infectious Disease and Immunology, Faculty of Medicine, Laval University, Québec G1V 4G2, Canada
Author contributions: Hui W made the review of the literature, wrote the manuscript, and prepared the figure; Bourgoin SG supervised the writing and made important revisions related to the content of the manuscript.
Supported by A research grant from the Arthritis Society of Canada, No. RG10/011 (to Bourgoin SG).
Conflict-of-interest statement: Authors declare no conflict of interest for this article.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Sylvain G Bourgoin, PhD, Division of Infectious Disease and Immunity, CHU de Québec Research Center and Department of Microbiology-Infectious Disease and Immunology, Faculty of Medicine, Laval University, 2705 Boul Laurier, Québec G1V 4G2, Canada. sylvain.bourgoin@crchudequebec.ulaval.ca
Received: May 29, 2015 Peer-review started: June 1, 2015 First decision: August 4, 2015 Revised: September 10, 2015 Accepted: October 16, 2015 Article in press: October 19, 2015 Published online: December 9, 2015
Core Tip
Core tip: Extracellular signal-regulated kinases 1/2 and p38 mitogen activated protein kinase cascades are activated in response to stimulation with inflammatory stimuli, including lysophosphatidic acid, and are able to activate mitogen- and stress-activated kinase (MSK) 1 and MSK2 in human synovial fibroblasts. MSKs then phosphorylate the transcription factor cAMP response element-binding protein (CREB), leading to the production of pro-inflammatory and anti-inflammatory cytokines. In addition to CREB, many other downstream effectors of MSK1/2 such as nuclear factor-kappa B, histone H3, the E3 ubiquitin ligase, Tripartite motif containing 7 and high mobility group nucleosome binding domain 1 have been reported and suggested to play important functions in immunity and disease states, including arthritis.
