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Updated: Mar 1, 2026
Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
Published on: March 18, 2022
miR-138 suppressed the progression of osteoarthritis mainly through targeting p65
1Department of Orthopaedics, Sir Run Run Hospital Nanjing Medical University, Nanjing, Jiangsu Province, China. wangzijian8686@163.com.
Objective:
MicroRNAs are reported to play key roles in regulating the main risk factors for osteoarthritis (OA) chondrogenesis. In the current study, we focused on miR-138, which has never been explored in OA.
Patients And Methods:
The expression of miR-138 and p65 was explored in the cartilage tissues of OA patients and compared with those of normal controls. We then explored the effects of miR-138 on NF-κB signaling activation in both human OA chondrocytes and chondrogenic SW1353 cells in the presence of 10 nM TNFα. The protein levels of p65, COX-2 and IL6 were determined using Western blot analysis. To validate the target gene of miR-138, a dual luciferase reporter assay was performed.
Results:
The level of miR-138 was markedly reduced in the OA cartilage tissues compared with those of normal controls. Real-time PCR analysis demonstrated that the level of miR-138 decreased after TNFα treatment for 3, 6, and 12 h in the normal chondrocytes and OA chondrocytes. Furthermore, overexpression of miR-138 suppressed the protein levels of p65, COX-2 and IL6 in human OA chondrocytes and chondrogenic SW1353 cells. A dual luciferase reporter assay demonstrated that miR-138 significantly suppressed the relative luciferase activity of pmirGLO-p65-3'UTR. More importantly, treatment with TNFα significantly enhanced the protein levels of p65, COX-2 and IL6. However, overexpression of miR-138 could partially abolish such effects.
Conclusions:
We demonstrated that reduced miR-138 expression enhanced the destruction of the cartilage tissues among OA patients, mainly through targeting p65.
Insights
Reduced miR-138 levels in osteoarthritis cartilage enhance tissue destruction by targeting p65. Restoring miR-138 may protect against osteoarthritis progression.
Area of Science:
- Biochemistry
- Molecular Biology
- Cell Biology
Background:
- MicroRNAs regulate key risk factors in osteoarthritis (OA) chondrogenesis.
- The role of miR-138 in OA pathogenesis remains unexplored.
Purpose of the Study:
- Investigate the role of miR-138 in OA.
- Determine the effect of miR-138 on NF-κB signaling pathway activation in OA chondrocytes.
Main Methods:
- Compared miR-138 and p65 expression in OA and normal cartilage.
- Utilized TNFα treatment in human OA chondrocytes and SW1353 cells.
- Performed Western blot analysis for p65, COX-2, and IL6 protein levels.
- Conducted dual luciferase reporter assay to validate miR-138 targets.
Main Results:
- miR-138 levels were significantly reduced in OA cartilage.
- Overexpression of miR-138 suppressed p65, COX-2, and IL6 protein levels.
- miR-138 directly targeted p65, as shown by luciferase assay.
- TNFα treatment increased p65, COX-2, and IL6, an effect partially abolished by miR-138 overexpression.
Conclusions:
- Reduced miR-138 expression contributes to cartilage destruction in OA.
- miR-138 targets p65, thereby modulating NF-κB signaling in OA chondrocytes.
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