ArticleExperimental and molecular pathology2014
Structural changes in hair follicles and sebaceous glands of hairless mice following exposure to sulfur mustard.
Article in Experimental and molecular pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Dermal Exposure to Vesicating Nettle Agent Phosgene Oxime: Clinically Relevant Biomarkers and Skin Injury Progression in Murine Models.The Journal of pharmacology and experimental therapeutics · 2024Article
- Skin Models Used to Define Mechanisms of Action of Sulfur Mustard.Disaster medicine and public health preparedness · 2023Review
- Article
- Skin remodeling and wound healing in the Gottingen minipig following exposure to sulfur mustard.Experimental and molecular pathology · 2020Article
- DNA damage signaling in the cellular responses to mustard vesicants.Toxicology letters · 2020Article
- Sulfur mustard induced mast cell degranulation in mouse skin is inhibited by a novel anti-inflammatory and anticholinergic bifunctional prodrug.Toxicology letters · 2018Article
- Tissue injury and repair following cutaneous exposure of mice to sulfur mustard.Annals of the New York Academy of Sciences · 2016Review
- Mustard vesicants alter expression of the endocannabinoid system in mouse skin.Toxicology and applied pharmacology · 2016Article
- Mitigation of nitrogen mustard mediated skin injury by a novel indomethacin bifunctional prodrug.Experimental and molecular pathology · 2016Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Sulfur mustard (SM) is a bifunctional alkylating agent causing skin inflammation, edema and blistering. A hallmark of SM-induced toxicity is follicular and interfollicular epithelial damage. In the present studies we determined if SM-induced structural alterations in hair follicles and sebaceous glands were correlated with cell damage, inflammation and wound healing. The dorsal skin of hairless mice was treated with saturated SM vapor. One to seven days later, epithelial cell karyolysis within the hair root sheath, infundibulum and isthmus was apparent, along with reduced numbers of sebocytes. Increased numbers of utriculi, some with connections to the skin surface, and engorged dermal cysts were also evident. This was associated with marked changes in expression of markers of DNA damage (phospho-H2A.X), apoptosis (cleaved caspase-3), and wound healing (FGFR2 and galectin-3) throughout pilosebaceous units. Conversely, fatty acid synthase and galectin-3 were down-regulated in sebocytes after SM. Decreased numbers of hair follicles and increased numbers of inflammatory cells surrounding the utriculi and follicular cysts were noted within the wound 3-7 days post-SM exposure. Expression of phospho-H2A.X, cleaved caspase-3, FGFR2 and galectin-3 was decreased in dysplastic follicular epidermis. Fourteen days after SM, engorged follicular cysts which expressed galectin-3 were noted within hyperplastic epidermis. Galectin-3 was also expressed in basal keratinocytes and in the first few layers of suprabasal keratinocytes in neoepidermis formed during wound healing indicating that this lectin is important in the early stages of keratinocyte differentiation. These data indicate that hair follicles and sebaceous glands are targets for SM in the skin.
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Registered trials
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