Circular RNA hsa_circ_0084054 promotes the progression of periodontitis with diabetes via the miR-508-3p/PTEN axis
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Updated: Jul 29, 2025

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
Published on: January 21, 2020
Linlin He1,2, Chengcheng Liu1,2, Yiying Liu1,2
1State Key Laboratory of Oral Diseases, & National Clinical Research Center for Oral Diseases, West China School of Stomatology, Sichuan University, Chengdu, China.
Background And Objective:
Diabetes is an important risk factor for periodontitis, and circular RNA (circRNA) may play an important role in aggravating inflammation and accelerating disease progression by regulating miRNA/mRNA. This study aimed to investigate the role and mechanism of the hsa_circ_0084054/miR-508-3p/PTEN axis in the progression of periodontitis with diabetes.
Methods:
First, circRNA sequencing was used to screen the differentially expressed circRNAs of periodontal ligament cells (PDLCs) treated with high glucose and/or Porphyromonas gingivalis lipopolysaccharide (LPS) in vitro, and the overtly differentially expressed hsa_circ_0084054 was selected and was also verified in periodontal ligament (PDL) tissue from periodontitis patients with diabetes. Then, its ring structure was tested by Sanger sequencing, RNase R, and actinomycin D assays. The bioinformatics analysis, dual luciferase reporter assay, and RIP assay were used to explore the interaction of hsa_circ_0084054/miR-508-3p/PTEN axis, whose effects on inflammation, oxidative stress, and apoptosis of PDLCs were evaluated through the measurement of inflammatory factors, reactive oxygen species (ROS), total superoxide dismutase (SOD), malondialdehyde (MDA), and Annexin V/PI assay.
Results:
By high-throughput sequencing, it was found that hsa_circ_0084054 was significantly increased in HG + LPS group compared with control group and LPS group, which was also verified in periodontal ligament (PDL) tissue from periodontitis patients with diabetes. Silencing hsa_circ_0084054 in PDLCs decreased the expression of inflammatory factors (IL-1β, IL-6, TNF-α), the levels of ROS and MDA, and the proportion of apoptotic cells; conversely, SOD activity was enhanced. In addition, we found that hsa_circ_0084054 could up-regulate the expression of PTEN through sponge miR-508-3p to inhibit AKT phosphorylation, finally trigger the aggravation of oxidative stress and inflammation in periodontitis patients with diabetes.
Conclusion:
hsa_circ_0084054 can aggravate inflammation and promote the progression of periodontitis with diabetes by regulating miR-508-3p/PTEN signaling axis, which may serve as a new target for the intervention of periodontitis with diabetes.
Insights
Circular RNA hsa_circ_0084054 exacerbates inflammation and oxidative stress in periodontitis with diabetes. It targets miR-508-3p to upregulate PTEN, promoting disease progression and potentially serving as a therapeutic target.
Area of Science:
- Molecular Biology
- Genetics
- Endocrinology
Background:
- Diabetes mellitus is a significant risk factor for periodontitis.
- Circular RNAs (circRNAs) are implicated in inflammatory processes and disease progression.
- The role of specific circRNAs, like hsa_circ_0084054, in the context of diabetes-associated periodontitis requires elucidation.
Purpose of the Study:
- To investigate the role and underlying mechanism of the hsa_circ_0084054/miR-508-3p/PTEN axis in periodontitis progression associated with diabetes.
- To identify potential molecular targets for therapeutic intervention.
Main Methods:
- circRNA sequencing identified differentially expressed circRNAs in periodontal ligament cells (PDLCs) under high glucose and lipopolysaccharide (LPS) conditions.
- In vitro and in vivo validation of hsa_circ_0084054 expression.
- Bioinformatics analysis, dual luciferase reporter assays, and RIP assays elucidated the interaction network.
- Assessment of cellular inflammation, oxidative stress, and apoptosis markers in PDLCs.
Main Results:
- hsa_circ_0084054 was significantly upregulated in high glucose + LPS treated PDLCs and in PDL tissues from diabetic periodontitis patients.
- Silencing hsa_circ_0084054 reduced inflammatory factors (IL-1β, IL-6, TNF-α), oxidative stress markers (ROS, MDA), and apoptosis, while enhancing SOD activity.
- hsa_circ_0084054 acts as a sponge for miR-508-3p, leading to PTEN upregulation, inhibited AKT phosphorylation, and aggravated inflammation and oxidative stress.
Conclusions:
- hsa_circ_0084054 plays a critical role in exacerbating inflammation and promoting the progression of periodontitis in diabetic patients.
- The hsa_circ_0084054/miR-508-3p/PTEN signaling axis is a key mechanism driving disease pathogenesis.
- hsa_circ_0084054 represents a promising novel therapeutic target for periodontitis associated with diabetes.
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