Research Paper Volume 13, Issue 18 pp 22490—22501
Nesfatin-1 facilitates IL-1β production in osteoarthritis synovial fibroblasts by suppressing miR-204-5p synthesis through the AP-1 and NF-κB pathways
- 1 Department of Veterinary Medicine, College of Veterinary Medicine, National Chung-Hsing University, Taichung, Taiwan
- 2 Department of Orthopedics, Taichung Veterans General Hospital, Taichung, Taiwan
- 3 School of Medicine, China Medical University, Taichung, Taiwan
- 4 Department of Medical Education and Research, China Medical University Beigang Hospital, Yunlin, Taiwan
- 5 Department of Sports Medicine, College of Health Care, China Medical University, Taichung, Taiwan
- 6 Department of Orthopedic Surgery, China Medical University Hospital, Taichung, Taiwan
- 7 Chinese Medicine Research Center, China Medical University, Taichung, Taiwan
- 8 Department of Medical Laboratory Science and Biotechnology, College of Medical and Health Science, Asia University, Taichung, Taiwan
Received: July 7, 2021 Accepted: September 7, 2021 Published: September 24, 2021
https://doi.org/10.18632/aging.203559How to Cite
Copyright: © 2021 Lee et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
The progression of osteoarthritis (OA) is mediated by adipokines, one of which is nesfatin-1, which is responsible for the production of inflammatory cytokines. However, how this molecule may affect the synthesis of the proinflammatory cytokine interleukin 1 beta (IL-1β) in OA is unclear. Our analyses of records from the Gene Expression Omnibus (GEO) dataset and clinical specimens of synovial tissue revealed higher levels of nesfatin-1 and IL-1β in OA samples compared with normal healthy tissue. We found that nesfatin-1 facilitates IL-1β synthesis in human OA synovial fibroblasts (OASFs) and suppresses the generation of micro-RNA (miR)-204-5p, as the miR-204-5p levels in OA patients were lower than those in healthy controls. Nesfatin-1-induced stimulation of IL-1β in human OASFs occurred via the suppression of miR-204-5p synthesis by the PI3K, Akt, AP-1 and NF-κB pathways. We suggest that nesfatin-1 is worth targeting in OA treatment.