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Arthritis Res Ther. 2018 Aug 3;20(1):163. doi: 10.1186/s13075-018-1660-6.

GPR120 is an important inflammatory regulator in the development of osteoarthritis.

Chen Y1,2,3, Zhang D4, Ho KW2, Lin S2,3, Suen WC2,5, Zhang H1, Zha Z1, Li G6,7, Leung PS8.

Author information

1
Institute of Orthopedic Diseases and Center for Joint Surgery and Sports Medicine, the First Affiliated Hospital, Jinan University, Guangzhou, People's Republic of China.
2
Department of Orthopaedics & Traumatology, Li Ka Shing Institute of Health Sciences and Lui Che Woo Institute of Innovative Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong SAR, People's Republic of China.
3
The CUHK-ACC Space Medicine Centre on Health Maintenance of Musculoskeletal System, The Chinese University of Hong Kong Shenzhen Research Institute, Shenzhen, People's Republic of China.
4
School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, Hong Kong SAR, People's Republic of China.
5
Department of Haematology, University of Cambridge, Cambridge, CB2 0PT, UK.
6
Department of Orthopaedics & Traumatology, Li Ka Shing Institute of Health Sciences and Lui Che Woo Institute of Innovative Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong SAR, People's Republic of China. gangli@cuhk.edu.hk.
7
The CUHK-ACC Space Medicine Centre on Health Maintenance of Musculoskeletal System, The Chinese University of Hong Kong Shenzhen Research Institute, Shenzhen, People's Republic of China. gangli@cuhk.edu.hk.
8
School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, Hong Kong SAR, People's Republic of China. psleung@cuhk.edu.hk.

Abstract

BACKGROUND:

The aim of this study was to investigate the regulatory role of G-protein coupled receptor 120 (GPR120) in the development and progression of osteoarthritis (OA).

METHODS:

GPR120 knockout (KO) and wild-type (WT) mice were used to create an animal model of OA by means of anterior cruciate ligament transection (ACLT) surgery. The severity of OA was staged and evaluated by histological examination, microcomputed tomography scan and enzyme-linked immunosorbent assay (ELISA). The anti-inflammatory effects of the GPR120 agonist docosahexaenoic acid (DHA) on human chondrocytes were further evaluated by specific inflammatory markers. In addition, the healing progression of a skin defect model was determined with histological assays.

RESULTS:

The GPR120-KO mice displayed an accelerated development of OA after ACLT. The secondary inflammation, cartilage degeneration, and subchondral bone aberrant changes were significantly elevated in the early phase of OA in KO mice relative to those in WT mice. In addition, we found that GPR120 levels were downregulated in OA patients compared with control subjects, whereas GPR120 activation with DHA exhibited anti-inflammatory effects in primary human chondrocytes in vitro. Moreover, results from the skin defect model showed that GPR120 agonism with DHA enhanced wound repair in mice, as shown by the downregulation of the number of CD68+ cells.

CONCLUSIONS:

Our study suggests that GPR120 is an important inflammatory mediator during the development of OA, and that it is a potential marker for the diagnosis of high-risk patients with OA.

KEYWORDS:

Cartilage; Diagnostic markers; G-protein coupled receptors; Polyunsaturated fatty acids; Proinflammatory mediators; Skin defect; Subchondral bone

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