Mus
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR165170_1.fastq.gz | Fastqsanger.gz | |||
| DRR165170_2.fastq.gz | Fastqsanger.gz | |||
| DRR165171_1.fastq.gz | Fastqsanger.gz | |||
| DRR165171_2.fastq.gz | Fastqsanger.gz | |||
| DRR165172_1.fastq.gz | Fastqsanger.gz |
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Project description:Diabetic nephropathy (DN) is the leading cause of dialysis and is associated with cardiovascular diseases. To prevent the progression of DN, not only glycemic control but also intervention to exacerbating factors such as chronic inflammation and infection. Recent clinical studies have shown the possible association between chronic kidney disease including DN, and periodontitis. However, the causal relationship that periodontitis could contribute to the progression of DN and its molecular mechanisms has not been understood. In the present study, we investigated ligature-induced experimental periodontitis that might exacerbate glomerular pathology in a DN model KK-Ay mice and the underlying molecular mechanisms. KK-Ay mice with experimental periodontitis showed significantly increased urinary albumin to creatinine ratio, and glomerular pathologies such as glomerular size, mesangial expansion area, fibrotic area, and number of CD68-positive leukocytes compared to those without ligatures. RNA-sequencing in the glomeruli revealed that hematopoietic prostaglandin d2 synthase (Hpgds) was the possible factor bridging periodontitis with the progression of DN. We also found that Hpgds expression was significantly upregulated by hyperglycemia and inflammatory stimuli in mesangial cells. Prostaglandin D2 enhanced hyperglycemia-induced collagen expression in mesangial cells and downregulated the tight junction in renal endothelial cells. Lastly, oral administration with an HPGDS inhibitor HQL-79 successfully prevented the progression of DN in KK-Ay mice by experimental periodontitis. Taken together, experimental periodontitis might contribute to the progression of DN via acceleration of glomerular pathology by upregulation of HPGDS in mesangial cells.
2025-05-03 | GSE261386 | GEO
Project description:Background/purpose Periodontal diseases exacerbate hepatic inflammation and diseases like non-alcoholic fatty liver disease via circulating pathogenic factors from periodontal tissue. Long-term pre-symptomatic state eventually leads to the development of such hepatic diseases. However, it is uncertain if periodontitis contributes in the onset of hepatic pre-symptomatic state. Herein, we conducted a hepatic whole transcription analysis of periodontitis-affected mice and healthy mice to understand the early functional changes in the hepatic system in periodontitis-affected mice. Materials and methods Silk ligatures were tied around mice second maxillary molars for 14 days to develop periodontitis. RNA-seq samples were collected from periodontal tissues and liver tissues of mice with periodontitis and healthy mice. Lipidomic analysis of hepatic omega-3 fatty acids in periodontitis-affected and healthy mice was conducted. The anti-inflammatory effects of omega-3 fatty acids and their metabolites were elucidated using hepatocytes HepG2 cells. Results In the liver of mice with periodontitis, genes coding for cytochrome P450 such as Cyp4a12a and Cyp4a12b were identified as significantly down-regulated genes. Lipidomic analyses identified that epoxidation and subsequent hydrolysis of hepatic omega-3 fatty acids were inhibited in periodontitis-affected mice. Eicosapentaenoic acid metabolites, epoxy eicosatetraenoic acid and dihydroxyeicosatetraenoic acid, inhibited inflammatory responses of HepG2 cells. Conclusion These results suggest that, in the liver of periodontitis-affected mice, due to the reduced activity of omega-3 fatty acid epoxidation, pre-symptomatic state with pro-inflammatory status develop. Therefore, early intervention of periodontitis might contribute to the prevention of the onset of hepatic diseases.
2024-05-03 | GSE264546 | 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:Purpose: The aim of this study was to explore whether differences exist and to what an extent of the immune-mediated inflammatory reactions between periodontitis and peri-implantitis at the transcriptional level in the same susceptible host. Methods: Ligature-induced experimental peri-implantitis and periodontitis in the same mice were established. Gingival tissues of healthy, periodontitis and peri-implantitis sites from the same oral cavity were collected and used for RNA-sequencing. Differentially expressed genes (DEGs) were screened between periodontitis/peri-implantitis sites and healthy sites. The enrichment analysis of DEGs were analyzed. Comprehensive immune landscape was annotated by seq-ImmuCC. Results: The results showed that 137 and 353 up-regulated DEGs as well as and 670 and 174 down-regulated DEGs were specifically expressed periodontitis/peri-implantitis group compared to the healthy control group, respectively. The pathways of complement and coagulation cascade and osteoclast differentiation were dominating in the peri-implantitis sites. Moreover, peri-implantitis sites exhibited elevated macrophage proportions and relatively enriched macrophage activation and bone loss compared with periodontitis. Conclusions: Results indicated that peri-implantitis and periodontitis exhibited significantly distinct transcriptional signatures. Additionally, the study suggests that the interplay between macrophages and bone resorption are comparatively more active in peri-implantitis compared with periodontitis. These biological processes may be factors contributing to the pathogenesis of peri-implantitis being distinct from that of periodontitis.
2022-06-06 | GSE186882 | GEO
Project description:Periodontitis patients often develop bacteremia, but there has been little evidence showing that oral bacteria translocate into other organs. We found that bacterial colony formation occurs in a culture of liver and spleen cells of periodontitis-induced mice, and the bacterial species detected in the liver and spleen were found in the oral cavity as well, but not in fecal samples, indicating systemic dissemination of oral bacteria during the breakdown of the oral barrier.
2018-01-26 | GSE109664 | GEO
Project description:scRNA-seq of gastrocnemius muscles from mice affected by periodontitis.
| PRJDB18430 | ENA
Project description:In order to determine the mechanism of the effect of periodontitis on the healing of tooth extraction sockets in mice, the mandibular first molar extraction models of mice in the periodontitis group and the control group were constructed respectively, and samples were taken for RNA-Seq at three time points: 0d, 3d, and 7d. Analysis of key genes in periodontitis regulating tooth extraction socket healing was conducted.
2025-07-31 | GSE248833 | GEO
Project description:Periodontitis patients exhibit significant upregulation of the cholinergic signaling pathway in gingival epithelial cells, accompanied by elevated acetylcholine (ACh) levels in saliva. However, the role of ACh in the pathogenesis of periodontitis remains unclear. P. gingivalis, a keystone pathogen in periodontitis, triggers host inflammatory responses and compromises the epithelial barrier function. As the first line of defense against pathogens, the reparative capacity of the oral epithelium critically influences the progression of periodontitis. This study investigates whether ACh modulates P. gingivalis-induced inflammatory responses and epithelial repair in human oral keratinocytes (HOKs), aiming to elucidate the mechanistic role of cholinergic signaling in periodontitis.
2025-05-21 | GSE297378 | GEO
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