Full Papers
FXR1 impedes the development of osteoarthritis by targeting SND1
H. Wang1, Z. Li2, L. Chen3, H. Lv4, Y. Sun5, F. Yan6, Y. Lu7
- Department of Radiology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
- Department of Radiology, Ruijin Hospital Luwan Branch, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
- Department of Radiology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
- Department of Radiology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
- Department of Radiology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
- Department of Radiology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
- Department of Radiology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, and Department of Radiology, Ruijin Hospital Luwan Branch, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. ly10936@rjh.com.cn
CER16404
2023 Vol.41, N°11
PI 2182, PF 2191
Full Papers
PMID: 37083155 [PubMed]
Received: 28/11/2022
Accepted : 03/03/2023
In Press: 06/04/2023
Published: 14/11/2023
Abstract
OBJECTIVES:
To investigate the role of fragile X mental retardation syndrome-related protein 1 (FXR1), an RNA binding protein, in the development of osteoarthritis (OA), to define its mechanism of action in cartilage, and to determine whether targeting FXR1 can prevent OA in mice.
METHODS:
Western blot analysis and quantitative polymerase chain reaction were performed using cartilage tissue from control and osteoarthritic mice. FXR1 expression was detected by immunofluorescence staining using cartilage tissue from mice. OA was induced by destabilising the medial meniscus in the mice. Infection of mouse chondrocytes with FXR1 lentivirus, as well as viral injection into the mouse knee joint cavity, resulted in high FXR1 protein expression. Chondrocyte apoptosis was detected by TUNEL assay and cell senescence was detected by SA-β-gal staining assay.
RESULTS:
FXR1 expression was significantly reduced in cartilage and soft tissue from mice with OA compared with the controls. FXR1 overexpression reduced staphylococcal nuclease domain protein 1 (SND1) levels. Furthermore, FXR1 is able to inhibit apoptosis and senescence of chondrocytes via SND1 and hinder the development of OA in mice.
CONCLUSIONS:
FXR1 down-regulates SND1 expression, thereby alleviating osteoarthritic symptoms in mice. In summary, FXR1 may have a therapeutic approach to the treatment of OA.
