ArticleFrontiers in cell and developmental biology2026
The LAMB3-ITGA6 axis orchestrates epithelial repair in periodontitis via hemidesmosomal regulation and keratinization modulation.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: Periodontitis manifests as dysregulated epithelial-stromal interactions and resultant tissue destruction, yet the regulatory mechanisms of the pivotal hemidesmosomes after periodontitis treatment remain elusive. Methodology: We utilized single-cell sequencing to profile the gene expression pattern of gingival epithelium in periodontitis patients with treatment. By adding retinol (keratinization inhibition) and BMS493 (keratinization promotion) in the human oral keratinocyte, we established and confirmed the Results: Seven distinct epithelial subpopulations were resolved, revealing a bifurcated repair trajectory where one fate selectively activates hemidesmosome-associated genes. In which, the LAMB3-ITGA6 axis emerged as a central hub for coordinating epithelial adhesion and strength. Retinoic acid reciprocally regulated this axis, with its pan-receptor antagonist BMS-493 accelerating epithelial cell keratinization. Importantly, the expressions of cytokeratin family were consistently downregulated in the LAMB3 knockdown group and upregulated in the LAMB3 overexpression group. Conclusion: This study identifying the LAMB3-ITGA6 axis as the target for promoting epithelial repair, which offer a precision medicine framework for periodontal healing.
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