Thioredoxin-1 promotes the restoration of alveolar bone in periodontitis with diabetes
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ABSTRACT:
PROVIDER: PRJNA988054 | ENA |
REPOSITORIES: ENA
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Project description:Treatment of periodontitis in people with diabetes remains challenging. Diabetes-enhanced oxidative stress is a primary cause of aggravation of periodontitis. The present study aimed to investigate the therapeutic potential of thioredoxin-1 (TRX1), an essential endogenous antioxidant protein, in the management of periodontitis with diabetes, as well as its role in modulating osteogenic differentiation. Our findings indicated that the production of reactive oxygen species (ROS) was elevated, while the expression of TRX1 was significantly reduced in the periodontal tissues of periodontitis mice with diabetes. Furthermore, knockdown of TRX1 in periodontal ligament stem cells (PDLSCs) resulted in the inhibition of osteogenic differentiation through disrupting Wnt/β-catenin signal pathway. However, this inhibition was restored upon administration of recombinant human TRX1 (rhTRX1). Importantly, rhTRX1 treatment decreased ROS generation, activated Wnt/β-catenin signal pathway and considerably promoted the alveolar bone repair of periodontitis mice with diabetes. These findings highlighted the crucial protective role of TRX1 in periodontitis with diabetes and suggested that it may serve as a potential therapeutic target for refractory periodontitis associated with oxidative stress.
2023-09-06 | GSE235930 | GEO
Project description:Treatment of periodontitis in people with diabetes remains challenging. The present study aimed to investigate the therapeutic potential of thioredoxin-1 (TRX1) in periodontitis with diabetes, as well as its role in modulating osteogenic differentiation. Our findings indicated that the production of reactive oxygen species (ROS) was elevated, while the expression of TRX1 was significantly reduced in the periodontal tissues of periodontitis mice with diabetes. Furthermore, knockdown of TRX1 in periodontal ligament stem cells (PDLSCs) resulted in the inhibition of osteogenic differentiation through disrupting Wnt/β-catenin signaling. However, this inhibition was restored upon administration of recombinant human TRX1 (rhTRX1). Importantly, rhTRX1 treatment decreased ROS generation, activated Wnt/β-catenin signal pathway and considerably promoted the alveolar bone repair of periodontitis mice with diabetes. These findings highlighted the crucial protective role of TRX1 in periodontitis with diabetes and suggested that it may serve as a potential therapeutic target for refractory periodontitis associated with oxidative stress.
| S-EPMC10470393 | biostudies-literature
Project description:To investigate the underlying mechanisms in the the states of apical periodontitis, we extracted RNA from control alveolar bone and alveolar bone under apical periodontitis.
2023-02-11 | GSE221990 | GEO
Project description:Salivary exsomal miRNAs may play important role in the pathogenesis of chronic inflammatory disease, such as periodontitis. There are many studies which suggested the connection between periodontitis and systemic disease, however, the role of specific miRNA as a intersection of periontitis and diabetes are not elucidated. We suggested miR-25-3p as possible common mediator in the pathogenesis of periodontitis and diabetes.
2021-11-20 | GSE189107 | GEO
Project description:Dysbiosis of subgingival microbiome promotes the growth of periodontopathogens and the development of periodontitis, an irreversible chronic inflammatory disease. Untreated periodontitis leads to the destruction of connective tissues, alveolar bone resorption and ultimately to tooth loss. Periodontitis has been associated with inflammatory metabolic diseases such as type 2 diabetes. While periodontitis-induced inflammation is a key player in both, the development of subgingival microbiome dysbiosis and in the host-microbiome interaction, the effects of hyperglycemia on the regulation of the host genes controlling the inflammatory response and the host-microbiome interaction are still scarce. We investigated the impacts of a hyperglycemic microenvironment on the inflammatory response and gene expression of a gingival fibroblasts-macrophages coculture model stimulated with dysbiotic subgingival microbiomes. A coculture model composed of immortalized human gingival fibroblasts overlaid with U937 macrophages-likes cells were stimulated with subgingival microbiome collected from four healthy donors and four patients with periodontitis. Pro-inflammatory cytokines and matrix metalloproteinase were measured by a Luminex assay while the coculture RNA was submitted to a microarray analysis. Subgingival microbiomes were submitted to 16s rRNA gene sequencing. Data were analyzed by using an advanced multi-omics bioinformatic data integration model. Our results showed that krt76, krt27, pnma5, mansc4, rab41, thoc6, tm6sf2, and znf506 as well as the pro-inflammatory cytokines IL-1, GM-CSF, FGF2, IL-10, the metalloproteinases MMP3 and MMP8, and bacteria from the ASV 105, ASV 211, ASV 299, Prevotella, Campylobacter and Fretibacterium genera are key correlated variables contributing to periodontitis-induced inflammatory response in a hyperglycemic microenvironment. To conclude, our multi-omics integration analysis unveiled unique differentially interrelated bacterial genera, genes and pro-inflammatory cytokines involved in the regulation of the inflammatory response in a hyperglycemic microenvironment. These data also highlight the importance of considering hyperglycemic conditions in the development of new drugs or treatments for periodontal disease in link with type 2 diabetes.
2023-05-31 | GSE222883 | GEO
Project description:Using single cell-RNA sequencing, we reported structural and functional changes of gingival cellulome in diabetes-associated periodontitis, with the aim to identify distinct cell populations and functions involving in disease progression. We identified inflammation-related stromal and epithelial subpopulations that expanded in diabetes-associated periodontitis, creating distinct immune microenvironment that drives the progression of the disease.
2023-09-11 | GSE189922 | GEO
Project description:In this study, an α2(VI) deficient mouse (Col6α2-KO) model was used to examine the role of Type VI collagen in oral tissues. To examine bone properties, µCT was employed, and bone volume and bone mineral density (BMD) was measured in oral tissues. To further investigate its molecular basis, proteome analysis was performed using protein extracted from alveolar bone. In addition, alveolar bone loss progression was evaluated with a periodontitis induced model. µCT analysis showed the Col6α2- KO mice had less volume of alveolar bone, dentin and dental pulp, while the width of periodontal ligament (PDL) was greater than WT. The BMD in alveolar bone and dentin were elevated in Col6α2-KO mice compared with WT. Our proteome analysis showed significant changes in proteins related to ECM organization and elevation of proteins associated with biomineralization in the Col6α2-KO mice. In induced periodontitis, Col6α2-KO mice had greater alveolar bone loss compared to WT. In conclusion, Type VI collagen has role in controlling biomineralization in alveolar bone and that changes in the ECM of alveolar bone could be associated with greater bone loss from periodontitis.
2022-11-21 | PXD037422 | Pride
Project description:The objective of this study is to investigate alveolar bone gene expression in health and diabetes through RNA-sequencing and bioinformatics analysis.
2021-10-01 | GSE182923 | GEO
Project description:RNA-seq analysis of RNA extracted from control alveolar bone samples and alveolar bone under apical periodontitis
| PRJNA917270 | ENA
Project description:Periodontitis (PD) as a chronic inflammatory disease instigated by periodontal pathogenic bacteria and mediated by the host immune response, resulting in the destruction of supporting periodontal tissue and tooth loss in adults. Constructing an injectable delivery system that allows for sustained drug release within periodontal pockets to continuously eliminate pathogenic bacteria, reduce periodontal inflammation, and promote periodontal tissue regeneration is an effective strategy for periodontitis treatment. Here, we explore the therapeutic potential and underlying mechanisms of curcumin-loaded Pickering emulsion (PE-CUR) in periodontitis treatment. The Pickering emulsion formulation offers an effective delivery system, enhancing curcumin's bioavailability and therapeutic efficacy. In vitro studies, we demonstrate that the PE-CUR exhibit excellent biocompatibility and anti-inflammatory property by elimination of reactive oxygen species (ROS). In addition, PE-CUR significantly eliminate key periodontal pathogens, including Porphyromonas gingivalis (P. gingivalis) and Staphylococcus aureus (S. aureus). In a rat model of periodontitis, PE-CUR significantly attenuates periodontal tissue inflammation and alveolar bone loss, indicating a protective effect against periodontal tissue destruction. Mechanistically, PE-CUR promotes the expression of anti-inflammatory factors and inhibits the release of pro-inflammatory factors by regulating macrophage polarization from M1 to M2 and modulating the MAPK and PI3K-AKT signaling pathway. Furthermore, PE-CUR decreases the formation of osteoclasts as well as stimulates the activation and differentiation of osteoblasts successively, thereby ameliorating the periodontal inflammation and promoting the alveolar bone regeneration. Overall, our findings elucidate the therapeutic mechanisms of PE-CUR in periodontitis, suggesting its potential as a promising treatment strategy warranting further clinical investigation.
2024-08-16 | GSE274645 | GEO