Journal of dermatological science最新文献

{"title":"RN7SL1 overexpression promotes cell proliferation in cutaneous T-cell lymphoma via miR-34a-5p/MYCN axis","authors":"Tingting Li ,&nbsp;Jiachen Sun ,&nbsp;Guanyu Wang ,&nbsp;Yimeng Wang ,&nbsp;Chunlei Zhang","doi":"10.1016/j.jdermsci.2025.03.003","DOIUrl":"10.1016/j.jdermsci.2025.03.003","url":null,"abstract":"<div><h3>Background</h3><div>Cutaneous T-cell lymphoma (CTCL) is a type of lymphoma that presents in skin tissue without evidence of extracutaneous disease. Emerging evidence indicates that long noncoding RNA-RN7SL1 serves as crucial effectors in modulating progression of different malignancies, including breast cancer, liver cancer, and other neoplasms.</div></div><div><h3>Objective</h3><div>To figure out the role of RN7SL1 in the pathogenesis of CTCL.</div></div><div><h3>Methods</h3><div>We detected RN7SL1 expression of CTCL patients by quantitative real-time polymerase chain reaction and fluorescent in situ hybridization. CTCL cell lines were transfected with lentiviral-based RN7SL1 gene knockdown vectors. Whole transcriptome sequencing was conducted to investigate differentially expressed miRNA and mRNA in CTCL, and we used qRT-PCR, RNA immunoprecipitation, dual-luciferase assay, RNA pull down and Western Blotting to further detect the relation of miRNA and mRNA. Also, we have verified above results in mice and clinical samples.</div></div><div><h3>Results</h3><div>LncRNA-RN7SL1 was overexpressed in CTCL compared with benign inflammatory dermatosis and was related to the TNMB stage of mycosis fungoides and Sézary syndrome (higher expression in IIB-IVB stage than IA-IIA stage). Additionally, the proliferation of CTCL cell lines HH and Hut78 was weakened, but apoptosis was facilitated by RN7SL1 downregulation, resulting in a reduced tumorigenic capacity in vivo. Subsequently, Whole transcriptome sequencing and target validation indicated that the RN7SL1/miR-34a-5p/MYCN axis may promoted malignant behavior in CTCL.</div></div><div><h3>Conclusion</h3><div>Our study suggested that RN7SL1 promoted malignant behavior by targeting miR-34a-5p/MYCN signaling. This finding might facilitate the discovery of novel biomarkers for CTCL diagnosis and treatment.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"118 1","pages":"Pages 18-28"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Topical sirolimus suppresses skin fibrosis in a bleomycin-induced mouse model of systemic sclerosis","authors":"Akiko Sekiguchi ,&nbsp;Mai Ishikawa ,&nbsp;Akihiko Uchiyama,&nbsp;Yoko Yokoyama,&nbsp;Sachiko Ogino,&nbsp;Ryoko Torii,&nbsp;Sei-ichiro Motegi","doi":"10.1016/j.jdermsci.2025.02.002","DOIUrl":"10.1016/j.jdermsci.2025.02.002","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"118 1","pages":"Pages 45-48"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143473339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A signal peptide variant in SLURP1 with dominant-negative effect causes progressive symmetric erythrokeratodermia","authors":"Zhuoqing Gong ,&nbsp;Yunran Peng ,&nbsp;Sisi Zhao ,&nbsp;Zhimiao Lin ,&nbsp;Zhanli Tang ,&nbsp;Huijun Wang","doi":"10.1016/j.jdermsci.2025.02.006","DOIUrl":"10.1016/j.jdermsci.2025.02.006","url":null,"abstract":"<div><h3>Background</h3><div>Progressive symmetric erythrokeratodermia (PSEK) is a group of hereditary cornification disorders characterized by symmetrical, progressive erythroderma and hyperkeratosis over the body. Loss-of-function variants in <em>SLURP1</em>, encoding secreted Ly-6/uPAR-related protein 1, is known to cause Mal de Meleda, an autosomal recessive palmoplantar keratoderma.</div></div><div><h3>Objective</h3><div>To identify the genetic basis and the pathogenesis of a sporadic patient with PSEK.</div></div><div><h3>Methods</h3><div>Whole-exome sequencing and Sanger sequencing were performed to identify the pathogenic variant(s). The expression of SLURP1 was assessed on the patient’s skin tissue by immunofluorescence. Western blotting (WB) and immunofluorescence (IF) were performed on eukaryotic overexpression systems to evaluate the signal peptide (SP) cleavage, subcellular localization and secretion of the mutant SLURP1. Combined WB and IF analyses were conducted on cells co-transfected with FLAG-tagged wild-type SLURP1 and untagged SLURP1-Ala22Asp.</div></div><div><h3>Results</h3><div>We identified a <em>de novo</em> heterozygous variant in <em>SLURP1</em> (c.65A &gt; C, p.Ala22Asp) affecting the first residue before SP cleavage site in a patient with PSEK. This variant abolished the cleavage site of SP, resulting in translocation deficiency to the Golgi apparatus and decreased secretion of the mutant SLURP1. We also found that the SLURP1-Ala22Asp exerted a dominant-negative effect by impeding the SP cleavage of the wild-type SLURP1 and affecting its subcellular localization and secretion in a dose-dependent manner.</div></div><div><h3>Conclusion</h3><div>We reported the first autosomal-dominant variant in <em>SLURP1</em> associated with a new phenotype of PSEK in a patient, emphasizing the genetic and clinical heterogeneity of <em>SLURP1</em>-associated genodermatoses.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"118 1","pages":"Pages 38-44"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143538267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thiotaurine inhibits melanoma progression by enhancing Ca2+ overload-induced cellular apoptosis","authors":"Di Wang ,&nbsp;Ansheng Xie ,&nbsp;Jialiang Luo ,&nbsp;Lei Li ,&nbsp;Zhiwen Zhang ,&nbsp;Weiwei Deng ,&nbsp;Bin Yang ,&nbsp;Yuan Chang ,&nbsp;Yunsheng Liang","doi":"10.1016/j.jdermsci.2025.03.001","DOIUrl":"10.1016/j.jdermsci.2025.03.001","url":null,"abstract":"<div><h3>Background</h3><div>Melanoma is the most dangerous type of skin cancer with poor therapy outcomes. Since malignant cells are more susceptible to Ca²⁺ overload than normal cells, activating Ca²⁺ overload-mediated apoptosis may be a promising strategy to inhibit melanoma progression. Hydrogen sulfide (H₂S) donors can regulate Ca²⁺ channels, but their effects on melanoma cells remain unclear.</div></div><div><h3>Objective</h3><div>To explore the effects of Thiotaurine (TTAU), an H₂S donor, on melanoma cells and its underlying mechanisms.</div></div><div><h3>Methods</h3><div>We tested the effect of TTAU by culturing melanoma cells in vitro and establishing the xenograft model of mice in vivo. Cell proliferation and apoptosis were assessed using the CCK-8 test and flow cytometry. Molecules involved in apoptosis or Ca²⁺-related signal transduction were analyzed by western blotting. Immunofluorescence was used to measure Ca²⁺ levels, mitochondrial damage, and reactive oxygen species (ROS).</div></div><div><h3>Results</h3><div>TTAU significantly reduced melanoma cell viability and induced apoptosis both in vitro and in vivo. Mechanistically, TTAU increased intracellular Ca²⁺, upregulated transient receptor potential vanilloid 1(TRPV1), and decreased activating transcription factor 3(ATF3) by nuclear factor of activated T cell cytoplasmic 1(NFATc1). TTAU also caused mitochondrial damage and ROS overproduction, which also promoted apoptosis.</div></div><div><h3>Conclusion</h3><div>We first elucidate that TTAU inhibits melanoma progression by activating Ca²⁺ influx-NFATc1-ATF3 signaling and aggravating mitochondrial oxidative stress, in which TRPV1 may act as an amplifier for Ca²⁺ influx. Our research is expected to provide new ideas for the treatment of tumors such as melanoma, as well as the clinical application of reactive sulfur species-based drugs.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"118 1","pages":"Pages 29-37"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143797289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Triclosan exacerbates atopic dermatitis in mouse models via thymic stromal lymphopoietin","authors":"Marie Charlotte Schuppe ,&nbsp;Patryk Porebski ,&nbsp;Katharina Klara Hahn ,&nbsp;Kexin Liao ,&nbsp;Anja Uhmann ,&nbsp;Andrea Braun ,&nbsp;Prasad Dasari ,&nbsp;Michael Peter Schön ,&nbsp;Timo Buhl","doi":"10.1016/j.jdermsci.2025.02.007","DOIUrl":"10.1016/j.jdermsci.2025.02.007","url":null,"abstract":"<div><h3>Background</h3><div>Triclosan, a common antimicrobial agent, is widely used in personal-care products and as a topical antiseptic in atopic dermatitis (AD).</div></div><div><h3>Objective</h3><div>This study aimed to evaluate the topical and systemic effect of triclosan on AD in murine models, with a specific focus on the role of thymic stromal lymphopoietin (TSLP).</div></div><div><h3>Methods</h3><div>AD-like skin disease was induced by topical application of MC903 and house dust mites in female wildtype BALB/c, C57BL/6 J, and TSLP receptor (TSLPR)-knockout mouse strains. Mice were treated with triclosan both topically and systemically. Skin inflammation was assessed by measuring ear thickness. Infiltration of immune cells was analyzed by flow cytometry and immunohistochemistry (IHC). Cytokine expression was determined by quantitative real-time PCR.</div></div><div><h3>Results</h3><div>Triclosan application induced skin inflammation in a dose-dependent manner. Topical triclosan treatment increased ear inflammation and immune cell infiltration in AD-like mouse models. Systemic administration of triclosan also enhanced local AD-like skin reactions. Triclosan-induced skin inflammation was reduced in TSLP-receptor-knockout mice or by blocking TSLP, thus indicating the pivotal role of TSLP in mediating the immunological effects of triclosan.</div></div><div><h3>Conclusions</h3><div>Topical and systemic administration of triclosan exacerbates AD-like skin inflammation in murine models, with TSLP being a central mediator of this process. The translational relevance of these findings to human disease remains uncertain, as no direct human data are available.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"118 1","pages":"Pages 1-8"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143588750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rapid thawing enhances tissue destruction in a mouse model of cutaneous cryoablation: Insights into oxidative stress and neutrophil activation","authors":"Akiko Sekiguchi ,&nbsp;Mai Ishikawa ,&nbsp;Akihiko Uchiyama ,&nbsp;Yoko Yokoyama ,&nbsp;Sachiko Ogino ,&nbsp;Ryoko Torii ,&nbsp;Ryoko Akai ,&nbsp;Takao Iwawaki ,&nbsp;Sei-ichiro Motegi","doi":"10.1016/j.jdermsci.2025.02.003","DOIUrl":"10.1016/j.jdermsci.2025.02.003","url":null,"abstract":"<div><h3>Background</h3><div>Cryoablation is an integral therapeutic approach in dermatology for eliminating viral warts and benign tumors by damaging tissue through freeze-thaw cycles. Rapid thawing of the frozen area by warming it with fingertips during cryoablation is a common technique in Japan; however, its efficacy has not been elucidated.</div></div><div><h3>Objective</h3><div>This study aimed to evaluate the effect of rapid thawing on cryoablation-treated skin and clarify the underlying mechanisms using cryoablation model mice.</div></div><div><h3>Methods</h3><div>Cryoablation was performed on the dorsal skin of mice using a liquid nitrogen-soaked cotton swab, followed by rapid thawing by warming with fingertips or natural thawing without treatment. The effects on skin ulcers, immune cell infiltration, and oxidative stress were assessed.</div></div><div><h3>Results</h3><div>Rapid thawing enlarged cryoablation-induced skin ulcers. The numbers of cryoablation-induced CD3⁺ T cells, neutrophils, neutrophil extracellular traps (NETs), and TUNEL⁺ cells increased with rapid thawing. Visualization of oxidative stress in OKD48 transgenic mice showed that oxidative stress signals in the cryoablation-treated area were enhanced with rapid thawing. Real-time PCR analysis of mouse skin demonstrated that cryoblation-induced levels of NOX2 and HO-1 were significantly elevated with rapid thawing. In mouse melanoma tumors treated with cryoablation, rapid thawing significantly inhibited tumor growth and increased the infiltration of neutrophils, NETs, and TUNEL⁺ cells compared to the group without rapid thawing.</div></div><div><h3>Conclusion</h3><div>Rapid thawing during cryoablation enhances neutrophil and lymphocyte infiltration, increases oxidative stress, and induces cell death, leading to greater tissue destruction in mice. Dermatologists should consider employing rapid thawing techniques during cryoablation when higher therapeutic intensities are required.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"118 1","pages":"Pages 9-17"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143506666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editors Choice","authors":"","doi":"10.1016/S0923-1811(25)00052-0","DOIUrl":"10.1016/S0923-1811(25)00052-0","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"118 1","pages":"Page ii"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143842778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"JSID’s Fellowship Shiseido Research Grant","authors":"","doi":"10.1016/S0923-1811(25)00054-4","DOIUrl":"10.1016/S0923-1811(25)00054-4","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"118 1","pages":"Page 49"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143842564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immune signatures across different stages of cutaneous squamous cell carcinoma.","authors":"Laure Favot-Laforge, Elodie Muzotte, Walid Mahfouf, Jerome Rambert, Muriel Cario, François Moisan, Lea Dousset, Hamid-Reza Rezvani","doi":"10.1016/j.jdermsci.2025.03.002","DOIUrl":"https://doi.org/10.1016/j.jdermsci.2025.03.002","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143775248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetics and epigenetics in vitiligo","authors":"Ken Okamura,&nbsp;Tamio Suzuki","doi":"10.1016/j.jdermsci.2025.01.004","DOIUrl":"10.1016/j.jdermsci.2025.01.004","url":null,"abstract":"<div><div>Vitiligo, a complex autoimmune disorder characterized by melanocyte destruction, arises from an intricate interplay of genetic, epigenetic, immune, and environmental factors. Genome-wide association studies (GWAS) have identified over 50 susceptibility loci, including key genes within the MHC region and those involved in immunity, oxidative stress, and melanogenesis. Concurrently, epigenetic research has unraveled regulatory networks critical to vitiligo pathogenesis, with a focus on DNA methylation and non-coding RNAs (e.g., microRNAs, long non-coding RNAs, and circular RNAs). These advancements provide deeper insights into gene regulation, immune processes, and cellular dynamics. This review integrates findings from genetic and epigenetic studies to offer a comprehensive understanding of molecular mechanisms of vitiligo, paving the way for innovative, personalized therapeutic approaches.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"117 3","pages":"Pages 45-51"},"PeriodicalIF":4.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143076758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}