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Peer-reviewedCC BY-NC-ND 4.0Purinergic Signalling

Single-cell transcriptomic analysis reveals fibroblast state-specific remodeling of purinergic signaling in diabetic gingiva

  • Sonia Batan1
  • Erivan S. Ramos-Junior1
  • Ana Carolina Morandini1,2
  1. 1Department of Oral Biology, Dental College of Georgia at Augusta University, Augusta, GA USA
  2. 2Department of Periodontics, Dental College of Georgia at Augusta University, Augusta, GA USA
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Abstract

Diabetes mellitus increases the risk and severity of periodontitis by disrupting periodontal mucosa homeostasis and promoting sustained chronic inflammation. Gingival fibroblasts are central regulators of periodontal integrity through extracellular matrix remodeling, immune modulation, and tissue repair. Purinergic signaling is an evolutionarily conserved pathway that regulates cellular metabolism and inflammatory responses, yet its role across distinct gingival fibroblast states in diabetes remains poorly understood. To address this gap, a publicly available single-cell RNA sequencing (scRNA-seq) dataset from wild-type (WT) and diabetic db/db mouse gingival tissue was analyzed. Fibroblasts were reclustered to identify transcriptionally distinct states, and genes associated with extracellular nucleotide signaling, adenosine signaling, ATP release, and inflammasome-associated pathways, including those related to Nlrp3 inflammasome. Genes were evaluated using differential expression, dot plots, UMAP feature plots, and state-specific log2 fold-change analyses. Four transcriptionally distinct fibroblast states were identified. Diabetic gingiva exhibited an expansion of the inflammatory fibroblast state accompanied by a reduction in ECM remodeling fibroblasts. Genes associated with extracellular nucleotide metabolism and adenosine signaling showed fibroblast state–specific expression patterns, including diabetes-associated differences in Nt5e (CD73), Entpd1 (CD39), and Enpp1 expressions. The adenosine receptor genes Adora2a and Adora2b were expressed at comparatively low levels. Genes associated with ATP release, including connexin-43 (Gja1) and pannexin-1 channels (Panx1), also displayed distinct state-specific expression patterns. Canonical inflammasome-associated genes were generally expressed at low levels, with Nek7 showing the highest overall expression and Casp11 exhibiting state-specific differences in expression, including a higher expression in selected diabetic fibroblast states. These findings identify an expansion of inflammatory fibroblasts in diabetic gingiva and characterize diabetes-associated changes in the expression of genes involved in extracellular nucleotide and nucleoside signaling, ATP release, and inflammasome-associated pathways that vary across fibroblast states.

Graphical Abstract:

Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1007/s11302-026-10195-x.

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Cite

BibTeXRIS
BibTeX
@article{batan2026singlecell,
  title = {{Single-cell transcriptomic analysis reveals fibroblast state-specific remodeling of purinergic signaling in diabetic gingiva}},
  author = {Sonia Batan and Erivan S. Ramos-Junior and Ana Carolina Morandini},
  journal = {Purinergic Signalling},
  year = {2026},
  month = oct,
  doi = {10.1007/s11302-026-10195-x},
  url = {https://doi.org/10.1007/s11302-026-10195-x},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Single-cell transcriptomic analysis reveals fibroblast state-specific remodeling of purinergic signaling in diabetic gingiva
AU  - Sonia Batan
AU  - Erivan S. Ramos-Junior
AU  - Ana Carolina Morandini
PY  - 2026
DA  - 2026/10/31
JO  - Purinergic Signalling
DO  - 10.1007/s11302-026-10195-x
UR  - https://doi.org/10.1007/s11302-026-10195-x
AB  - Diabetes mellitus increases the risk and severity of periodontitis by disrupting periodontal mucosa homeostasis and promoting sustained chronic inflammation. Gingival fibroblasts are central regulators of periodontal integrity through extracellular matrix remodeling, immune modulation, and tissue repair. Purinergic signaling is an evolutionarily conserved pathway that regulates cellular metabolism and inflammatory responses, yet its role across distinct gingival fibroblast states in diabetes remains poorly understood. To address this gap, a publicly available single-cell RNA sequencing (scRNA-seq) dataset from wild-type (WT) and diabetic db/db mouse gingival tissue was analyzed. Fibroblasts were reclustered to identify transcriptionally distinct states, and genes associated with extracellular nucleotide signaling, adenosine signaling, ATP release, and inflammasome-associated pathways, including those related to Nlrp3 inflammasome. Genes were evaluated using differential expression, dot plots, UMAP feature plots, and state-specific log2 fold-change analyses. Four transcriptionally distinct fibroblast states were identified. Diabetic gingiva exhibited an expansion of the inflammatory fibroblast state accompanied by a reduction in ECM remodeling fibroblasts. Genes associated with extracellular nucleotide metabolism and adenosine signaling showed fibroblast state–specific expression patterns, including diabetes-associated differences in Nt5e (CD73), Entpd1 (CD39), and Enpp1 expressions. The adenosine receptor genes Adora2a and Adora2b were expressed at comparatively low levels. Genes associated with ATP release, including connexin-43 (Gja1) and pannexin-1 channels (Panx1), also displayed distinct state-specific expression patterns. Canonical inflammasome-associated genes were generally expressed at low levels, with Nek7 showing the highest overall expression and Casp11 exhibiting state-specific differences in expression, including a higher expression in selected diabetic fibroblast states. These findings identify an expansion of inflammatory fibroblasts in diabetic gingiva and characterize diabetes-associated changes in the expression of genes involved in extracellular nucleotide and nucleoside signaling, ATP release, and inflammasome-associated pathways that vary across fibroblast states.  Graphical Abstract:  Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1007/s11302-026-10195-x.
SN  - 1573-9538
SN  - 1573-9546
ER  -