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Updated: Feb 28, 2026
Three-dimensional Inflammatory Human Tissue Equivalents of Gingiva
Published on: April 3, 2018
MicroRNA-126 Regulates Inflammatory Cytokine Secretion in Human Gingival Fibroblasts Under High Glucose via Targeting
Yi Wu1, Li-Ting Song1, Jia-Shan Li1
1Department of Stomatology, Hospital of Stomatology, School of Dentistry, Tianjin Medical University, Tianjin, China.
Background:
MicroRNAs (miRs) play a crucial role in inflammatory diseases, including periodontitis. Meanwhile, miRs act as biomarkers for predicting diabetes mellitus (DM). However, the regulatory mechanism of miR-126 on development of periodontitis in patients with DM still remains unclear.
Methods:
Human gingival fibroblasts were cultured with low (5.5 mmol/L), medium (15 mmol/L), and high (25 mmol/L) glucose, respectively. Expressions of miR-126, tumor necrosis factor (TNF) receptor associated factor (TRAF) 6, and related cytokines were analyzed by real-time polymerase chain reaction (PCR). After transfection with miR-126 mimic, PCR and western blot were performed to detect level of TRAF6, and luciferase reporter assay confirmed if TRAF6 is the direct target of miR-126. Production of cytokines was measured using enzyme-linked immunosorbent assay.
Results:
Increased glucose significantly suppressed miR-126 expression in human gingival fibroblasts (P <0.05). Also, high glucose increased TRAF6, interleukin (IL)-6, TNF-α, and chemical chemokine ligand (CCL) 2 levels, whereas it decreased IL-10 level. MiR-126 mimic significantly decreased TRAF6 mRNA and protein levels under high glucose (P <0.05). Also, miR-126 directly targeted TRAF6 through binding to its 3' untranslated region in human gingival fibroblasts. Overexpression of miR-126 significantly abrogated high glucose-induced secretion of proinflammatory cytokines such as IL-6, TNF-α, and CCL2 and promoted production of IL-10.
Conclusion:
These data suggest that miR-126 inhibits inflammation of human gingival fibroblasts under high glucose through targeting TRAF6, which may be a potential therapeutic target for periodontitis concomitant with DM.
Insights
MicroRNA-126 (miR-126) inhibits inflammation in human gingival fibroblasts under high glucose conditions by targeting TRAF6. This finding offers a potential therapeutic strategy for periodontitis in diabetes mellitus patients.
Area of Science:
- Biochemistry
- Molecular Biology
- Immunology
Background:
- MicroRNAs (miRs) are implicated in inflammatory diseases like periodontitis.
- miRs serve as biomarkers for predicting diabetes mellitus (DM).
- The regulatory role of miR-126 in periodontitis associated with DM is not well understood.
Purpose of the Study:
- To investigate the mechanism by which miR-126 regulates periodontitis in patients with DM.
- To explore the relationship between glucose levels, miR-126 expression, and inflammatory markers in human gingival fibroblasts.
Main Methods:
- Human gingival fibroblasts were exposed to varying glucose concentrations.
- Expression levels of miR-126, TRAF6, and cytokines were quantified using RT-PCR and ELISA.
- Luciferase reporter assays confirmed the direct targeting of TRAF6 by miR-126.
Main Results:
- Elevated glucose suppressed miR-126 expression and increased pro-inflammatory cytokines (IL-6, TNF-α, CCL2) while decreasing IL-10.
- Overexpression of miR-126 reduced TRAF6 mRNA and protein levels under high glucose conditions.
- miR-126 directly targeted TRAF6 and abrogated high glucose-induced inflammation.
Conclusions:
- miR-126 inhibits inflammation in human gingival fibroblasts under high glucose by targeting TRAF6.
- This miR-126/TRAF6 pathway represents a potential therapeutic target for periodontitis in patients with DM.
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