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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

Yat-Yin Law1,2, Yu-Min Lin1,3, Shan-Chi Liu4, Min-Huan Wu5,6, Wen-Hui Chung7, Chun-Hao Tsai8,9, Yi-Chin Fong8,10, Chih-Hsin Tang7,11,12, Chin-Kun Wang13
  • 1Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan
  • 2Department of Orthopedics, Chung Shan Medical University Hospital, Taichung, Taiwan
  • 3Department of Orthopedic Surgery, Taichung Veterans General Hospital, Taichung, Taiwan
  • 4Department of Medical Education and Research, China Medical University Beigang Hospital, Yunlin, Taiwan
  • 5Physical Education Office, Tunghai University, Taichung, Taiwan
  • 6Sports Recreation and Health Management Continuing Studies, Tunghai University, Taichung, Taiwan
  • 7Department of Pharmacology, School of Medicine, China Medical University, Taichung, Taiwan
  • 8Department of Sports Medicine, College of Health Care, China Medical University, Taichung, Taiwan
  • 9Department of Orthopedic Surgery, China Medical University Hospital, Taichung, Taiwan
  • 10Department of Orthopedic Surgery, China Medical University Beigang Hospital, Yunlin, Taiwan
  • 11Chinese Medicine Research Center, China Medical University, Taichung, Taiwan
  • 12Department of Biotechnology, College of Health Science, Asia University, Taichung, Taiwan
  • 13School of Nutrition, Chung Shan Medical University, Taichung, Taiwan
Received: February 15, 2020Accepted: June 29, 2020Published: September 29, 2020
https://doi.org/10.18632/aging.103889

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.