Single-cell Transcriptomic Atlas of Gingival Mucosa in Type 2 Diabetes
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ABSTRACT:
PROVIDER: PRJNA777932 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16775200_1.fastq.gz | Fastqsanger.gz | |||
| SRR16775200_2.fastq.gz | Fastqsanger.gz | |||
| SRR16775201_1.fastq.gz | Fastqsanger.gz | |||
| SRR16775201_2.fastq.gz | Fastqsanger.gz | |||
| SRR16775202_1.fastq.gz | Fastqsanger.gz |
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Project description:The oral gingival barrier is a constantly stimulated and dynamic environment where homeostasis is often disrupted, resulting in inflammatory periodontal diseases. Type 2 diabetes (T2D), a risk factor for periodontitis, has been reported to be associated with barrier dysfunction, but the effect and underlying mechanism are inconclusive. Herein, we performed single-cell RNA sequencing (scRNA-seq) of gingiva from leptin receptor-deficient (db/db) mice to understand the heterogeneity of gingival barrier in the context of T2D. Periodontal health of control mice is characterized by populations of Krt14+-expressing epithelial cells and Col1a1+-fibroblasts mediating immune homeostasis primarily through the enrichment of innate lymphoid cells. The db/db mice exhibit an impaired gingival barrier with spontaneous periodontal bone loss, and a decreased proportion of epithelial/stromal cells. We further observed stromal, particularly fibroblast immune hyperresponsiveness linked to recruitment of myeloid cell populations in gingiva from T2D mice. Analysis of ligand-receptor interaction pairs suggested inflammatory signaling between fibroblasts and myeloid cells, a main driver of diabetes-induced periodontal damage. Moreover, the “Immune-like” stromal cells contributed to gingival Th17/IL-17 hyperresponsiveness in T2D. Our work reveals transcriptional diversity of stromal cells and interaction with innate immune cells in T2D, and uncovers the “immune-like” fibroblast subsets participating in barrier homeostasis at the diabetic gingiva.
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Project description:The onset of periodontitis involves the response of gingival stroma to inflammatory stimulus. The cell constitution of gingival stroma, however, has never been mapped at the resolution of single cell. In this study, we used single-cell mRNA sequencing to establish cell atlas in mouse gingival stroma. Epithelial, mesenchymal, pericyte and neuronal clusters were successfully identified and their subpopulation and response to ligature-induced inflammation were also examined. While shifts in epithelial cell gene profile and proportion recapitulated the epithelium breakdown during periodontitis, mesenchymal cluster maintained its proportion and gene expression patterns.
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Project description:Oral mucosa of smokers is subject to cigarette smoke (CS)-related cytological, genomic, and transcriptional changes that could potentially lead to the development of mouth diseases. In order to further characterize CS effects, we took advantage of two human organotypic in vitro models of the buccal and gingival epithelia (MatTek(R)) that have been developed from the same donor (healthy, non-smoker) to reflect the in vivo situation. Both gingival and buccal organotypic cultures were exposed to fresh, diluted CS at the air-liquid interface in parallel and 4 times (one conventional reference cigarette 3R4F at a time, 1 h intervals, CS dilution with air: 0.46 L/min or 0.16 L/min resulting in CS concentrations of 19.7% and 40.7% (v/v) respectively. Gene expression was captured at time 0 h following the 4th exposure and after different post-exposure time points (4h, 24h, 48h) to investigate time- and concentration-dependent CS effect on both tissues. Other endpoints (e.g. cytotoxicity, pro-inflammatory marker release, cytochrome P450 (CYP) activity, immunohistology) were also measured for some time points. By using computational approaches and by capturing systems biology endpoints, various perturbations of biological processes (e.g. inflammation, cell proliferation, cellular stress) triggered by repeated exposure to CS were analyzed in both buccal and gingival in vitro models. We describe here for the first time the impact of whole CS exposure on human buccal and gingival organotypic in vitro models using various approaches combining systems biology, biological network models, computational methods and standard endpoints.
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