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Updated: Feb 16, 2026
Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
Published on: March 18, 2022
The lncRNA MEG3 downregulation leads to osteoarthritis progression via miR-16/SMAD7 axis
Jin Xu1,2, Yaozeng Xu1
1Department of Orthopedics, The First Affiliated Hospital of Soochow University, No. 899 Ping Hai Road, Gusu District, Suzhou, 215031 China.
Background:
Osteoarthritis (OA) is a chronic joint disease and there is no a definitive cure at present. Long non-coding RNAs (lncRNAs) have been confirmed to play important roles in the development of OA. However, the underlying mechanism of lncRNA maternally expressed gene 3 (MEG3) in OA has not been well elucidated.
Methods:
The rat OA model and interleukin-1β (IL-1β)-induced rat chondrocytes were constructed. The expression pattern of lncRNA MEG3 and miR-16 was detected by RT-qPCR assay in cartilage tissues of rat OA model. The effect of MEG3 and miR-16 on IL-1β-induced chondrocytes was evaluated on the basis of cell viability and apoptosis. Then, the interaction among MEG3, miR-16 SMAD7 was explored by dual-luciferase reporter assay and RIP assay.
Results:
It is found that lncRNA MEG3 was down-regulated and miR-16 was up-regulated in rat OA cartilage tissues. MEG3 knockdown promoted proliferation and inhibited apoptosis, while miR-16 knockdown suppressed proliferation and promoted apoptosis in IL-1β-induced rat chondrocytes. Moreover, MEG3 was involved in miR-16 pathway and MEG3 suppressed miR-16 expression. Additionally, SMAD7 was a target gene of miR-16 and miR-16 suppressed SMAD7 expression in IL-1β-induced chondrocytes. Moreover, the expression of SMAD7 induced by MEG3 or si-MEG3 was markedly reversed by the introduction of miR-16 or anti-miR-16. Furthermore, MEG3 exerted its anti-proliferation and pro-apoptosis by regulating miR-16 and SMAD7.
Conclusion:
MEG3 was down-regulated and miR-16 was up-regulated in cartilage tissues of rat OA model. MEG3 knockdown might lead to the progression of OA through miR-16/SMAD7 axis.
Insights
Osteoarthritis progression may be linked to reduced long non-coding RNA MEG3 levels. This study reveals MEG3 influences OA by regulating the miR-16/SMAD7 pathway in chondrocytes.
Area of Science:
- Molecular Biology
- Genetics
- Biochemistry
Background:
- Osteoarthritis (OA) is a prevalent degenerative joint condition with no current cure.
- Long non-coding RNAs (lncRNAs) are implicated in OA pathogenesis, but the role of maternally expressed gene 3 (MEG3) remains unclear.
Purpose of the Study:
- To investigate the role and mechanism of lncRNA MEG3 in osteoarthritis.
- To elucidate the interaction between MEG3, miR-16, and SMAD7 in OA development.
Main Methods:
- Established a rat model of osteoarthritis and used IL-1β-induced rat chondrocytes.
- Quantified MEG3 and miR-16 expression using RT-qPCR.
- Assessed cell viability and apoptosis, and explored molecular interactions via dual-luciferase and RIP assays.
Main Results:
- MEG3 was downregulated, while miR-16 was upregulated in OA cartilage.
- MEG3 knockdown enhanced chondrocyte proliferation and inhibited apoptosis; miR-16 knockdown had opposite effects.
- MEG3 negatively regulated miR-16, which in turn suppressed SMAD7 expression.
Conclusions:
- MEG3 downregulation and miR-16 upregulation are observed in OA cartilage.
- MEG3 may promote OA progression by modulating the miR-16/SMAD7 axis.
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