ArticleCell death & disease2024
Targeting miR-497-5p rescues human keratinocyte dysfunction upon skin exposure to sulfur mustard.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The trial behind it
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Who cites it
4 citing papers in PubMed.
- Nitrogen Mustard Disrupts Bioenergetics and Activates Oxidative Stress-Induced Cell Death Pathways in Human Keratinocytes.Chemical research in toxicology · 2026Article
- HypoxamiRs: the hidden architects of tissue adaptation in hypoxia.Cell death & disease · 2025Review
- Microneedle-aided nanotherapeutics delivery and nanosensor intervention in advanced tissue regeneration.Journal of nanobiotechnology · 2025Review
- Exosomal miR-493-3p Promote the Secretion of CXCL10 by Suppressing Keratinocyte Autophagy in Vitiligo.Clinical, cosmetic and investigational dermatology · 2025Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Sulfur mustard (SM) is a highly toxic chemical warfare agent. Exposure to SM results in various pathologies including skin lesions with subsequent impaired wound healing. To date, there are no effective treatments available. Here we discover a SM-triggered pathomechanism involving miR-497-5p and its target survivin which contributes to keratinocyte dysfunction. Transcriptome analysis using RNA-seq in normal human epidermal keratinocytes (NHEK) revealed that SM evoked differential expression of 1896 mRNAs and 25 miRNAs with many of these RNAs known to be involved in keratinocyte function and wound healing. We demonstrated that keratinocyte differentiation and proliferation were efficiently regulated by miRNAs induced in skin cells after exposure to SM. The inhibition of miR-497-5p counteracted SM-induced premature differentiation and stimulated proliferation of NHEK. In addition, we showed that microneedle-mediated transdermal application of lipid-nanoparticles containing miR-497-5p inhibitor restored survivin biosynthesis and cellular functionality upon exposure to SM using human skin biopsies. Our findings expand the current understanding of SM-associated molecular toxicology in keratinocytes and highlight miR-497-5p as feasible clinical target for specific skin therapy in SM-exposed patients and beyond.
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Registered trials
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