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Updated: Aug 2, 2025
Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
Published on: March 18, 2022
FXR1 impedes the development of osteoarthritis by targeting SND1
Hanqi Wang1, Zhihui Li2, Liuping Chen1
1Department of Radiology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
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.
Insights
Fragile X mental retardation syndrome-related protein 1 (FXR1) is reduced in osteoarthritis (OA). FXR1 overexpression inhibits chondrocyte apoptosis and senescence, potentially offering a therapeutic strategy for OA treatment.
Area of Science:
- Biochemistry
- Molecular Biology
- Orthopedics
Background:
- Osteoarthritis (OA) is a degenerative joint disease.
- The role of RNA binding proteins in OA pathogenesis is not fully understood.
- FXR1 is an RNA binding protein implicated in various cellular processes.
Purpose of the Study:
- To investigate the role of FXR1 in OA development.
- To elucidate the mechanism of FXR1 action in cartilage.
- To assess the therapeutic potential of targeting FXR1 in an OA mouse model.
Main Methods:
- Western blot, qPCR, and immunofluorescence staining were used to assess FXR1 expression in mouse OA models.
- OA was induced by destabilizing the medial meniscus.
- Chondrocyte apoptosis and senescence were evaluated using TUNEL and SA-β-gal assays, respectively.
Main Results:
- FXR1 expression was significantly decreased in OA cartilage and soft tissues.
- FXR1 overexpression reduced staphylococcal nuclease domain protein 1 (SND1) levels.
- FXR1 inhibited chondrocyte apoptosis and senescence, and hindered OA progression in mice.
Conclusions:
- FXR1 down-regulates SND1 expression, alleviating OA symptoms in mice.
- FXR1 demonstrates potential as a therapeutic target for OA treatment.
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