Research Paper Volume 12, Issue 18 pp 18635—18648
Visfatin increases ICAM-1 expression and monocyte adhesion in human osteoarthritis synovial fibroblasts by reducing miR-320a expression
- 1 Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan
- 2 Department of Orthopedics, Chung Shan Medical University Hospital, Taichung, Taiwan
- 3 Department of Orthopedic Surgery, Taichung Veterans General Hospital, Taichung, Taiwan
- 4 Department of Medical Education and Research, China Medical University Beigang Hospital, Yunlin, Taiwan
- 5 Physical Education Office, Tunghai University, Taichung, Taiwan
- 6 Sports Recreation and Health Management Continuing Studies, Tunghai University, Taichung, Taiwan
- 7 Department of Pharmacology, School of Medicine, China Medical University, Taichung, Taiwan
- 8 Department of Sports Medicine, College of Health Care, China Medical University, Taichung, Taiwan
- 9 Department of Orthopedic Surgery, China Medical University Hospital, Taichung, Taiwan
- 10 Department of Orthopedic Surgery, China Medical University Beigang Hospital, Yunlin, Taiwan
- 11 Chinese Medicine Research Center, China Medical University, Taichung, Taiwan
- 12 Department of Biotechnology, College of Health Science, Asia University, Taichung, Taiwan
- 13 School of Nutrition, Chung Shan Medical University, Taichung, Taiwan
Received: February 15, 2020 Accepted: June 29, 2020 Published: September 29, 2020
https://doi.org/10.18632/aging.103889How to Cite
Copyright: © 2020 Law 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
Pathophysiological events that modulate the progression of structural changes in osteoarthritis (OA) include monocyte adhesion and infiltration, and synovial inflammation. In particular, the adhesion protein intercellular adhesion molecule type 1 (ICAM-1) promotes monocyte recruitment into the synovial tissue. Visfatin is an adipocyte hormone that promotes the release of inflammatory cytokines during OA progression. We report that visfatin enhances ICAM-1 expression in human OA synovial fibroblasts (OASFs) and facilitates the adhesion of monocytes with OASFs. AMPK and p38 inhibitors, as well as their respective siRNAs, attenuated the effects of visfatin upon ICAM-1 synthesis and monocyte adhesion. We also describe how miR-320a negatively regulates visfatin-induced promotion of ICAM-1 expression and monocyte adhesion. We detail how visfatin affects ICAM-1 expression and monocyte adhesion with OASFs by inhibiting miR-320a synthesis via the AMPK and p38 signaling pathways.