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:Emerging evidence indicates that gingival-resident helper CD4+ T cells are major drivers of periodontal inflammation in response to commensal and pathogenic oral microorganisms. Whether tissue-resident memory CD8+ T cells (TRM), which principally safeguard against viruses and cancer but also drive certain autoimmune and inflammatory conditions, impact periodontitis progression and severity remain unknown. We asked whether local reactivation of oral CD8+ TRM of a defined antigen specificity could exacerbate ligature-induced periodontitis (LIP), a well-established model of periodontal disease in mice. Topical application of virus-mimicking peptides to the oral mucosa concurrent with LIP 1) intensified alveolar bone loss, 2) amplified gingival and cervical lymph node inflammation, and 3) stimulated gingival transcriptional changes in genes related to innate immune sensing and cell-mediated cytotoxicity. Therapeutic depletion of CD103-expressing oral CD8+ TRM in advance of LIP prevented exacerbation of disease. These observations provide evidence that oral CD103+ CD8+ TRM have the potential to participate in gingival inflammation, alveolar bone loss, and periodontitis.
2026-04-10 | GSE293729 | GEO
Project description:Ligature-induced periodontitis (LIP) induces rapid alveolar bone loss followed by gingival immunosuppressive conditions
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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.
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Project description:Aim: To clarify the molecular mechanisms of occlusal trauma in bone loss through periodontal tissue transcriptome analysis in mice with periodontitis and traumatic occlusion. Materials and Methods: Ligature-induced periodontitis (Li) and composite resin-induced traumatic occlusion (Tra) mouse models were established: control (Co), Li, Tra, and LiTra. Bone resorption was evaluated using micro-computed tomography (micro-CT). RNA sequencing (RNA-seq) was conducted on gingiva, bone, and periodontal ligament from all groups 3 days post-induction. For long-term evaluation, the Co and Tra groups were maintained for 8 weeks, then analyzed using micro-CT and qRT-PCR. Results: Traumatic occlusion alone, sustained for 8 weeks, did not directly induce bone resorption; however, it significantly exacerbated bone resorption in mice with periodontitis. Cytokine–cytokine receptor interactions and Toll-like receptor signaling pathways were upregulated in LiTra bone tissue. Il11, Il1rl1, and Mmp3, associated with inflammation and bone metabolism, were more highly expressed in the LiTra group than in the Li group. TNF-α signaling via NFκB and inflammatory response gene sets were enriched in the bone tissue of LiTra group. Conclusions: Traumatic occlusion accelerates bone resorption in ligature-induced periodontitis but does not independently cause significant bone loss. Occlusal trauma enhances the expression of inflammation-related genes especially in bone with periodontitis.
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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 is an inflammatory condition affecting periodontal tissues, such as the gingiva and alveolar bone, surrounding the teeth. However, previous research has focused on analyzing a single sample type, such as tissue, blood, or gingival crevicular fluid (GCF), which may limit the comprehensive understanding of the complex pathology of periodontitis. We conducted a proteomic analysis using liquid chromatography-mass spectrometry (LC-MS) on the periodontal tissues and GCF from patients with periodontitis. This analysis distinguished distinct proteomic signatures between the two sample types, with 3,803 proteins being identified in periodontal tissue and 910 proteins in GCF, underscoring the significant variances pertinent to periodontal health. Proteins such as S100A12, MPO, APOA1, CTSG, and PSMA1 were markedly upregulated in GCF, suggesting their potential as key markers of neutrophil activity and systemic inflammation. These findings provide profound insights into both the local and systemic pathophysiological processes underlying periodontitis, emphasizing the utility of GCF as a non-invasive medium for reflecting comprehensive disease states.
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