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Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
Published on: March 18, 2022
CircSCAPER knockdown attenuates IL-1β-induced chondrocyte injury by miR-127-5p/TLR4 axis in osteoarthritis
Yuchang Zhang1, Ping Zhao1, Sen Li1
1Department of Orthopedics, Gansu Provincial Hospital of Traditional Chinese Medicine, Lanzhou, China.
Purpose:
Osteoarthritis (OA) is a chronic inflammatory degenerative disease characterized by articular cartilage degradation. Circular RNAs have been shown to play significant roles in OA process. Herein, this work aimed to investigate the potential role and mechanism of circSCAPER in OA progression.
Methods:
Levels of circSCAPER, miR-127-5p and toll-like receptor 4 (TLR4) were detected by qRT-PCR or western blotting. Cell apoptosis was determined by flow cytometry. The expression of Aggrecan and Matrix metallopeptidase was examined using western blot to assess extracellular matrix (ECM) degradation. Inflammatory response and oxidative stress were determined by measuring the release of inflammatory factors, along with the generation of intracellular reactive oxygen species and malondialdehyde. The interaction between miR-127-5p and circSCAPER or TLR4 was determined by dual-luciferase reporter, RNA immunoprecipitation and pull-down assays.
Results:
Chondrocytes were treated with interleukin-1β (IL-1β) to mimic OA condition in vitro. CircSCAPER was increased in OA cartilages and IL-1β-induced chondrocytes. Functionally, knockdown of circSCAPER attenuated IL-1β-evoked apoptosis, ECM degradation, inflammation and oxidative stress in vitro. CircSCAPER up-regulation in OA cartilages was discovered to be accompanied by decreased miR-127-5p and increased TLR4. Mechanistically, circSCAPER acted as a sponge for miR-127-5p to positively regulate TLR4 expression in chondrocytes. IL-1β treatment reduced miR-127-5p expression but up-regulated TLR4 expression, re-expression of miR-127-5p suppressed IL-1β-caused chondrocyte injury, which was abolished by TLR4 overexpression. Moreover, miR-127-5p inhibition reversed the protective action of circSCAPER knockdown on chondrocytes under IL-1β treatment.
Conclusion:
CircSCAPER silencing protected against IL-1β-induced apoptosis, ECM degradation, inflammation and oxidative stress in chondrocytes via miR-127-5p/TLR4 axis.
Insights
Circular RNA circSCAPER promotes osteoarthritis progression by increasing apoptosis, extracellular matrix degradation, inflammation, and oxidative stress. Silencing circSCAPER offers a protective effect against these osteoarthritis-related damages.
Area of Science:
- Biochemistry
- Molecular Biology
- Cell Biology
Background:
- Osteoarthritis (OA) is a degenerative joint disease characterized by articular cartilage breakdown.
- Circular RNAs (circRNAs) are implicated in the pathogenesis of OA.
Purpose of the Study:
- To investigate the role and mechanism of circSCAPER in osteoarthritis progression.
- To elucidate the circSCAPER/miR-127-5p/TLR4 regulatory axis in OA.
Main Methods:
- Quantitative real-time PCR and Western blotting to measure circSCAPER, miR-127-5p, and TLR4 levels.
- Flow cytometry for apoptosis assessment; Western blot for ECM degradation markers.
- Dual-luciferase reporter, RNA immunoprecipitation, and pull-down assays to confirm molecular interactions.
Main Results:
- CircSCAPER expression was elevated in OA cartilage and IL-1β-treated chondrocytes.
- Knockdown of circSCAPER reduced IL-1β-induced apoptosis, ECM degradation, inflammation, and oxidative stress.
- CircSCAPER sponged miR-127-5p, leading to increased TLR4 expression, exacerbating chondrocyte injury.
Conclusions:
- CircSCAPER silencing demonstrates a protective effect against IL-1β-induced chondrocyte injury.
- The miR-127-5p/TLR4 axis is a key mechanism through which circSCAPER influences OA pathogenesis.
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