Ontology highlight
ABSTRACT:
PROVIDER: PRJNA639904 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12031057_1.fastq.gz | Fastqsanger.gz | |||
| SRR12031057_2.fastq.gz | Fastqsanger.gz | |||
| SRR12031058_1.fastq.gz | Fastqsanger.gz | |||
| SRR12031058_2.fastq.gz | Fastqsanger.gz | |||
| SRR12031059_1.fastq.gz | Fastqsanger.gz |
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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: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.
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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
Project description:Background: Periodontitis is a chronic inflammatory disease and macrophages play a pivotal role in the progression of periodontitis. Mesenchymal stem cells (MSCs) have emerged as potential therapeutic agents for the treatment of periodontitis due to their immunomodulatory properties and capacity for tissue regeneration. Compared to conventionally derived MSCs, induced pluripotent stem cell-derived MSCs (iMSCs) offer distinct advantages as promising candidates for MSC-based therapies, owing to their non-invasive acquisition methods and virtually unlimited availability. This study aims to investigate the effects and mechanisms of iMSCs in modulating macrophage polarization and alleviating periodontitis-related alveolar bone loss. Methods: iMSCs were generated from iPSCs and characterized for differentiation potential. The effects of iMSCs on macrophage polarization were evaluated using THP-1-derived macrophages under inflammatory conditions (LPS and IFN-γ stimulation). Co-culture assays, cytokine analysis, reactive oxygen species (ROS) detection, transcriptomic analysis, flow cytometry, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and western blot analysis were performed to elucidate the underlying mechanisms. The therapeutic potential of iMSCs was assessed in a ligature-induced periodontitis mouse model using micro-CT, histological analysis, and immunofluorescence staining. Results: iMSCs inhibit M1 macrophage polarization through the suppression of the NF-κB signaling pathway. Additionally, iMSCs reduce the production of pro-inflammatory cytokines (IL-1β, IL-17) and reactive oxygen species (ROS), while enhancing the secretion of anti-inflammatory cytokines (IL-10) and growth factors (VEGF), thereby improving the inflammatory microenvironment. Under inflammatory conditions, iMSCs preserve the osteogenic potential of periodontal ligament stem cells (PDLSCs) and alleviate alveolar bone loss in mice with periodontitis. In vivo, iMSCs reduce the number of M1 macrophages and inhibit the activation of NF-κB in periodontal tissues, supporting their anti-inflammatory and immunomodulatory effects. Conclusion: iMSCs demonstrate significant therapeutic potential in periodontitis by modulating macrophage polarization, reducing oxidative stress, and mitigating alveolar bone loss associated with the disease. These findings provide new insights into the mechanisms of iMSCs and their application as cell-based therapies for periodontal diseases.
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Project description:Periodontitis and type Ⅱ diabetes mellitus (T2D) have emerged as prevalent global chronic diseases, with a bidirectional relationship existing between them. Individuals with periodontitis and T2D are susceptible to tooth loss, primarily attributed to alveolar bone resorption resulting from excessive osteoclasts (OC) differentiation. Although low-intensity pulsed ultrasound (LIPUS) is an established treatment method for bone-related conditions, its mechanism of action on OC remains unclear. The aim of this research is to examine the effects and mechanism of on OC within a diabetic inflammatory environment. In summary, our data explored how LIPUS affects OC in the inflammatory environment of diabetes.
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Project description:The iTRAQ method was used to analyze differences in protein expression in alveolar bone tissue during the progression of apical periodontitis in rats.
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Project description:Saccharibacteria (TM7) are obligate epibionts living on the surface of their host bacteria, and strongly correlated with dysbiotic microbiomes during periodontitis and other inflammatory diseases, suggesting they are putative pathogens. However, due to the recalcitrance of TM7 cultivation, no causal research has been conducted to investigate their role in inflammatory diseases. Here, we isolated multiple TM7 species on their host bacteria from periodontitis patients. These TM7 species reduced inflammation and consequential bone loss by modulating their host bacterial pathogenicity in mouse ligature-induced periodontitis model. Two host bacterial functions involved in collagen binding and utilization of eukaryotic sialic acid were identified as required for inducing bone loss and altered by TM7 association. This down-regulation of host bacterial pathogenicity by TM7 was shown for multiple TM7/host bacteria pairs, suggesting that, in contrast to their suspected pathogenic role, TM7 could protect mammalian hosts from inflammatory damage induced by their host bacteria.
2023-03-11 | PXD026999 | Pride
Project description:Neutrophil recruitment and activation are hallmarks of the prevalent inflammatory disease, periodontitis. However, the mechanisms by which neutrophils contribute to in inflammatory bone destruction remain unclear. Herein, we document that neutrophil extracellular traps (NETs) have a direct role in mediating inflammatory pathology. In an established animal model of periodontitis, we demonstrate that genetic or pharmacologic inhibition of NETs formation, or removal of NETs by DNase-Ⅰ, alleviates inflammatory bone loss in vivo. Investigating the mechanisms by which NETs drive periodontal inflammation, we find that extracellular histones have a direct role in disease progression. Consistent with findings in animal models, histones bearing classic NET-associated post-translational modifications are correlated with disease severity and are significantly elevated in local lesions and systemic circulation of patients with periodontitis. Our work reveals NETs-associated components as pathogenic mediators, potential biomarkers, and therapeutic targets for periodontitis.
2023-05-23 | GSE228021 | GEO
Project description:Healthy alveolar bone is the cornerstone for oral function and oral treatment. In the aging population, increasingly postmenopausal women requiring dental services experiences alveolar bone loss due to estrogen deficiency. Both local factors (occlusal force lose) and systemic factors (estrogen deficiency) affects their alveolar bone health, but the association remains to be clarified. Here, we identified that occlusal force is critical in maintaining alveolar bone mass and PIEZO1 coordinates mechanical force and estrogen, thus orchestrating alveolar bone homeostasis. Mechanistically, both occlusal force loss and PIEZO1 deletion may impair the osteogenesis of alveolar bone and sequentially regulate catabolic metabolism through Fas ligand (FasL)-induced osteoclastic apoptosis. PIEZO1 may promote the activity of signal transducer and activator of transcription 3 (STAT3) and estrogen receptor 1 (ESR1), which cooperatively increase Fasl transcription. This study thus revealed a cooperation between occlusal force and estrogen in maintaining alveolar bone homeostasis through a PIEZO1-STAT3/ESR1-FasL pathway. Our work supports restoration of occlusal force with dental therapies early and suggests that preventing alveolar bone loss is the major priority. PIEZO1 may serve not only as a treatment target for occlusal force loss-induced alveolar bone loss but also as a potential target for metabolic bone loss, especially in older patients.
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