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Updated: Jul 20, 2025
Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
Published on: March 18, 2022
microRNA-105-5p protects against chondrocyte injury, extracellular matrix degradation, and osteoarthritis progression
Dong Jiang1, Shigao Cheng1, Pengcheng Kang1
1Department of Orthopedic Surgery, Loudi Central Hospital, Loudi, Hunan, PR China.
Objective:
Both microRNA (miR)-105-5p and SPARCL1 were discovered to be differentially expressed in osteoarthritis (OA), but their roles and exact mechanisms have not been entirely elaborated. This paper sets out to probe the impact of miR-105-5p/SPARCL1 on chondrocyte injury, extracellular matrix degradation, and osteoarthritis progression.
Methods:
C28/I2 cells were stimulated with IL-1β to construct an in vitro OA model. C28/I2 cells were transfected with sh-SPARCL1, oe-SPARCL1, or miR-105-5p mimic before IL-1β induction. CCK-8 assay, flow cytometry, and ELISA were adopted to assess cell viability, apoptosis, and inflammatory factor expression, respectively. The binding relationship of miR-105-5p to SPARCL1 was assessed using dual-luciferase reporter assay. After an OA rat model was established, rats underwent intra-articular injection with ago-miR-105-5p. TUNEL was applied to determine cell apoptosis in vivo. mRNA and protein levels were measured by qRT-PCR and western blot, respectively, in vitro and in vivo.
Results:
IL-1β treatment diminished miR-105-5p expression and augmented SPARCL1 expression in C28/I2 cells. miR-105-5p decreased SPARCL1 expression by targeting SPARCL1. miR-105-5p overexpression or SPARCL1 silencing prominently reversed the decrease in viability and the promotion of inflammatory factor production, cartilage matrix degradation, and apoptosis in IL-1β-stimulated C28/I2 cells. Furthermore, upregulation of SPARCL1 nullified the influence of miR-105-5p overexpression on viability, apoptosis, inflammation, and cartilage matrix degradation in IL-1β-stimulated C28/I2 cells. miR-105-5p overexpression ameliorated knee cartilage tissue injury in OA rats.
Conclusion:
Conclusively, miR-105-5p exerted suppressive effects on chondrocyte injury, extracellular matrix degradation, and OA progression by targeting SPARCL1.
Insights
MicroRNA (miR)-105-5p suppresses osteoarthritis progression by targeting SPARCL1. This study reveals miR-105-5p
Area of Science:
- Molecular Biology
- Cell Biology
- Biochemistry
Background:
- Osteoarthritis (OA) involves differential expression of miR-105-5p and SPARCL1.
- The precise roles and mechanisms of miR-105-5p and SPARCL1 in OA remain unclear.
Purpose of the Study:
- To investigate the impact of miR-105-5p and SPARCL1 on chondrocyte injury.
- To elucidate their roles in extracellular matrix degradation and OA progression.
Main Methods:
- An in vitro OA model using IL-1β-stimulated C28/I2 cells.
- Transfection with miR-105-5p mimics or SPARCL1-related vectors.
- Assessment of cell viability, apoptosis, and inflammation via CCK-8, flow cytometry, and ELISA.
- Dual-luciferase reporter assay to confirm targeting.
- In vivo study using an OA rat model with intra-articular miR-105-5p injection.
Main Results:
- IL-1β reduced miR-105-5p and increased SPARCL1 expression.
- miR-105-5p directly targeted and decreased SPARCL1 expression.
- miR-105-5p overexpression or SPARCL1 silencing protected against IL-1β-induced chondrocyte damage.
- SPARCL1 upregulation counteracted the protective effects of miR-105-5p.
- miR-105-5p overexpression improved cartilage integrity in OA rats.
Conclusions:
- miR-105-5p inhibits chondrocyte injury, extracellular matrix degradation, and OA progression.
- The suppressive effects are mediated through targeting SPARCL1.
