Journal
CELLULAR IMMUNOLOGY
Volume 315, Issue -, Pages 27-33Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.cellimm.2016.10.007
Keywords
Rheumatoid arthritis; Fibroblast-like synoviocytes; PDK1; RSK2
Categories
Funding
- National Basic Research Program of China (973 Program) [2012CB822104]
- National Natural Science Foundation of China [31170766, 81171140, 81202368]
- Clinical Medicine Special Funds of Jiangsu Province [BL2014059]
- Natural Science Foundation of Jiangsu Province [BK20150408]
- Key Project Natural Science Foundation of Jiangsu University and College [11KJA310002]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
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This study investigated the role of PDK1 in inflammatory response which is initiated by TNF-alpha and analyzed the association between PDK1 and RSK2. TNF-alpha were added into MH7A cells to induce inflammation condition. Through overexpressing or suppressing PDK1 in MH7A cells, the role of PDK1 in cell invasiveness and inflammatory factors was determined. Levels of MMPs protein and inflammatory cytokines were assessed with PDK1 siRNA and TNF-alpha treatment. Inhibition of RSK2 was used to investigate the function of RSK2 on PDK1-induced inflammation. The phosphorylation of RSK2 was detected when PDK1 was inhibited. Luciferase reporter assay was performed to detect the transcriptional activity of NF-kappa B. We found highly expressed PDK1 could promote cell invasion and secretion of IL-1 beta and IL-6 in MH7A cells. Inhibition of RSK2 reduced the PDK1-induced cell invasion and cytokines secretion in MH7A cells. In response to TNF-alpha, PDK1 could phosphorylate RSK2 and activated RSK2, then promoting the activation of NF-kappa B. This may be a possible therapeutic option of rheumatoid arthritis. (C) 2016 Elsevier Inc. All rights reserved.
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