ArticleAnnals of dermatology2025
Botulinum Toxin A Modulates Keratinocyte Proliferation and Inflammatory and Pruritic Mediators in Wound Healing.
Article in Annals of dermatology, 2025. 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
backgroundBotulinum toxin type A (BTA) is widely used in dermatologic procedures. While its anti-fibrotic effects on fibroblasts are well established, its role in keratinocyte-driven inflammation and pruritus during wound healing remains underexplored.
objectiveTo evaluate the effects of BTA on keratinocyte proliferation, migration, and transforming growth factor-beta (TGF-β)-induced expression of inflammatory and pruritus-associated mediator.
methodsHuman epidermal keratinocytes were stimulated with TGF-β to mimic wound conditions, followed by BTA co-treatment. Cell proliferation and migration were assessed using water soluble tetrazolium salt-8 and scratch assays. Western blotting evaluated Smad2/3 and extracellular signal-regulated kinase (ERK)1/2 phosphorylation. Reverse transcription-quantitative polymerase chain reaction was used to quantify inflammatory cytokines and itch-related mediators.
resultsBTA significantly enhanced keratinocyte proliferation without affecting migration. It inhibited TGF-β-induced phosphorylation of Smad2/3 and ERK1/2. BTA also downregulated pro-inflammatory cytokines (interleukin [IL]-1β, IL-6, tumor necrosis factor-α, monocyte chemotactic protein 1, prostaglandin E synthase) and pruritus-related mediators (IL-31, IL-33, cathepsin S, calcitonin gene-related peptide, substance P, and thymic stromal lymphopoietin).
conclusionBTA promotes keratinocyte proliferation and reduces TGF-β-induced inflammatory and pruritus-associated mediators. These findings suggest that BTA may facilitate wound healing by promoting keratinocyte proliferation while simultaneously modulating inflammation and pruritic responses.
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