gingival spatial transcriptomics data Search Results


gingival spatial transcriptomics data  (Spatial Transcriptomics Inc)
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Spatial Transcriptomics Inc gingival spatial transcriptomics data
Acetylcholine signaling and receptor distribution in the periodontal epithelium. (A) Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment of epithelial neurotransmitter signaling-related DEGs. Left: upregulated pathways in PD vs. HC; right: downregulated pathways in TP vs. PD. (B) Expression profiles of acetylcholine receptors across different cell types. Receptors not detected in any cells were excluded. (C) Transcript counts of acetylcholine receptor genes from HOKs RNA-seq data. Five receptors detected in all 12 samples (n = 3 per group), with colored shapes representing groups and black bars indicating the mean. Receptors with low expression (zero counts in some samples) were excluded. (D) Expression of acetylcholine receptors CHRNB1 , CHRNA5 , and CHRNA7 in gingival spatial <t>transcriptomics</t> data.
Gingival Spatial Transcriptomics Data, supplied by Spatial Transcriptomics Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Acetylcholine signaling and receptor distribution in the periodontal epithelium. (A) Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment of epithelial neurotransmitter signaling-related DEGs. Left: upregulated pathways in PD vs. HC; right: downregulated pathways in TP vs. PD. (B) Expression profiles of acetylcholine receptors across different cell types. Receptors not detected in any cells were excluded. (C) Transcript counts of acetylcholine receptor genes from HOKs RNA-seq data. Five receptors detected in all 12 samples (n = 3 per group), with colored shapes representing groups and black bars indicating the mean. Receptors with low expression (zero counts in some samples) were excluded. (D) Expression of acetylcholine receptors CHRNB1 , CHRNA5 , and CHRNA7 in gingival spatial transcriptomics data.

Journal: Frontiers in Cell and Developmental Biology

Article Title: Acetylcholine in the gingival epithelium drives the pathogenesis of periodontitis

doi: 10.3389/fcell.2025.1701252

Figure Lengend Snippet: Acetylcholine signaling and receptor distribution in the periodontal epithelium. (A) Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment of epithelial neurotransmitter signaling-related DEGs. Left: upregulated pathways in PD vs. HC; right: downregulated pathways in TP vs. PD. (B) Expression profiles of acetylcholine receptors across different cell types. Receptors not detected in any cells were excluded. (C) Transcript counts of acetylcholine receptor genes from HOKs RNA-seq data. Five receptors detected in all 12 samples (n = 3 per group), with colored shapes representing groups and black bars indicating the mean. Receptors with low expression (zero counts in some samples) were excluded. (D) Expression of acetylcholine receptors CHRNB1 , CHRNA5 , and CHRNA7 in gingival spatial transcriptomics data.

Article Snippet: Utilizing single-cell RNA sequencing (scRNA-seq) data (205,334 cells, 40 human gingival samples) and gingival spatial transcriptomics data (46,230–25 μm 2 spots), we revealed that the gingival epithelium exhibits the most significant functional reprogramming of neural signaling pathways in the periodontitis state.

Techniques: Expressing, RNA Sequencing

Distribution of tight junction genes in the periodontal gingival epithelium and their regulation by acetylcholine. (A) Expressions of OCLN, CLDN1, and CDH1 in spatial transcriptomics data. (B) Differential comparison of OCLN, CLDN1, and CDH1 in the epithelial subpopulation of HC versus PD groups (***, p < 0.001). (C) Heatmap showing the expressions of OCLN, CLDN1, and CDH1 for each cluster in HC and PD gingiva. (D) Quantitative polymerase chain reaction (qPCR) validation in HOKs. Data are presented as the mean ± standard error of the mean (SEM). ***, p < 0.001.

Journal: Frontiers in Cell and Developmental Biology

Article Title: Acetylcholine in the gingival epithelium drives the pathogenesis of periodontitis

doi: 10.3389/fcell.2025.1701252

Figure Lengend Snippet: Distribution of tight junction genes in the periodontal gingival epithelium and their regulation by acetylcholine. (A) Expressions of OCLN, CLDN1, and CDH1 in spatial transcriptomics data. (B) Differential comparison of OCLN, CLDN1, and CDH1 in the epithelial subpopulation of HC versus PD groups (***, p < 0.001). (C) Heatmap showing the expressions of OCLN, CLDN1, and CDH1 for each cluster in HC and PD gingiva. (D) Quantitative polymerase chain reaction (qPCR) validation in HOKs. Data are presented as the mean ± standard error of the mean (SEM). ***, p < 0.001.

Article Snippet: Utilizing single-cell RNA sequencing (scRNA-seq) data (205,334 cells, 40 human gingival samples) and gingival spatial transcriptomics data (46,230–25 μm 2 spots), we revealed that the gingival epithelium exhibits the most significant functional reprogramming of neural signaling pathways in the periodontitis state.

Techniques: Comparison, Real-time Polymerase Chain Reaction, Biomarker Discovery