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, Jiachen Sun, Guanyu Wang, Yimeng Wang, Chunlei Zhang","doi":"10.1016/j.jdermsci.2025.03.003","DOIUrl":"https://doi.org/10.1016/j.jdermsci.2025.03.003","url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Objective: </strong>To figure out the role of RN7SL1 in the pathogenesis of CTCL.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>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.</p>","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":"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":"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}

{"title":"Cytosolic mtDNA-cGAS-STING axis mediates melanocytes pyroptosis to promote CD8+ T-cell activation in vitiligo","authors":"Xinya Xu ,&nbsp;Xinhua Lu ,&nbsp;Yue Zheng ,&nbsp;Yang Xie ,&nbsp;Wei Lai","doi":"10.1016/j.jdermsci.2024.12.002","DOIUrl":"10.1016/j.jdermsci.2024.12.002","url":null,"abstract":"<div><h3>Background</h3><div>The cGAS-STING axis, a DNA sensor pathway, has recently emerged as a key hub in sensing stress signals and initiating the immune cascade in several diseases. However, its role in the pathogenesis of vitiligo remains unclear.</div></div><div><h3>Objective</h3><div>To explore the pathogenic role of the cGAS-STING axis in linking oxidative stress and CD8⁺ T-cell-mediated anti-melanocytic immunity in vitiligo.</div></div><div><h3>Methods</h3><div>The expression status of the cGAS-STING axis and cytosolic mtDNA were evaluated in the oxidatively stressed epidermal cells and vitiligo perilesional skin, respectively. Then, we investigated the activation of cGAS-STING axis in mtDNA-treated melanocytes, and the influence of cGAS or STING silencing on mtDNA-induced melanocytes pyroptosis. Finally, the paracrine effects of melanocytes pyroptosis on CD8⁺ T cell activation were explored.</div></div><div><h3>Results</h3><div>We initially demonstrated that the cGAS-STING axis in melanocytes was highly susceptible to oxidative stress and activated in the vitiliginous melanocytes of perilesional skin, accompanied by enhanced cytosolic mtDNA accumulation. Our mechanistic <em>in vitro</em> experiments confirmed that oxidative stress-induced mitochondrial damage in epidermal cells led to cytosolic mtDNA accumulation, which served as a trigger in activating the cGAS-STING axis in melanocytes. Furthermore, the cytosolic mtDNA-cGAS-STING axis was verified to mediate melanocytes pyroptosis. More importantly, we found that IL-1β and IL-18 produced by pyroptotic melanocytes promoted the activation of CD8⁺ T cells from patients with vitiligo.</div></div><div><h3>Conclusion</h3><div>The present study confirmed that the cytosolic mtDNA-cGAS-STING axis of melanocytes played an important role in oxidative stress-triggered CD8⁺ T-cell response, providing novel insights into mechanisms underlying vitiligo onset.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"117 3","pages":"Pages 61-70"},"PeriodicalIF":4.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143191565","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":"Unveiling intratumoral heterogeneity in high-risk cutaneous squamous cell carcinoma using single-cell spatial enhanced resolution omics-sequencing (Stereo-seq)","authors":"Jesse Veenstra ,&nbsp;Ian Loveless ,&nbsp;Peter Dimitrion ,&nbsp;Indra Adrianto ,&nbsp;David Ozog ,&nbsp;Qing-Sheng Mi","doi":"10.1016/j.jdermsci.2024.11.001","DOIUrl":"10.1016/j.jdermsci.2024.11.001","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"117 3","pages":"Pages 88-90"},"PeriodicalIF":4.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142792684","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":"Type 2 cytokine-JAK1 signaling is involved in the development of dry skin-induced mechanical alloknesis","authors":"Yui Toyosawa ,&nbsp;Eriko Komiya ,&nbsp;Takahide Kaneko ,&nbsp;Yasushi Suga ,&nbsp;Mitsutoshi Tominaga ,&nbsp;Kenji Takamori","doi":"10.1016/j.jdermsci.2024.10.002","DOIUrl":"10.1016/j.jdermsci.2024.10.002","url":null,"abstract":"<div><h3>Background</h3><div>Mechanical alloknesis (m-alloknesis) is itch hypersensitivity induced by normally innocuous stimuli. It is sometimes observed in dry skin based itch-related diseases such as atopic dermatitis (AD), and often triggers the vicious itch-scratch cycle. The acetone-ether and water (AEW) mouse model mimics dry skin-induced m-alloknesis, yet its underlying mechanism remains unclear. Janus kinase (JAK) inhibitors are used to treat AD, but their effects on m-alloknesis are not fully known.</div></div><div><h3>Objective</h3><div>To reveal the effects of various oral JAK inhibitors on m-alloknesis and their action points, using AEW model.</div></div><div><h3>Methods</h3><div>AEW model was prepared by treatment with a mixture of acetone-ether, and they were orally administrated a JAK1/2 inhibitor baricitinib, a selective JAK1 inhibitor abrocitinib, or a JAK2 selective inhibitor AZ960, and evaluated m-alloknesis score as the total number of scratching responses in 30 mechanical stimulations. To further elucidate the mechanism of action, IL-4, IL-13 or thymic stromal lymphopoietin (TSLP) or their neutralizing antibodies were also applied to mice. In addition, the levels of these cytokines in mouse skin were measured using multiple immunoassays.</div></div><div><h3>Results</h3><div>All of JAK inhibitors effectively reduced m-alloknesis, with abrocitinib demonstrating the most significant inhibition. The neutralizing antibodies against IL-4, IL-13, and TSLP inhibited m-alloknesis in AEW mice. Intradermal administration of IL-4, IL-13, or TSLP induced m-alloknesis, and abrocitinib effectively mitigated each cytokine-induced response. Highly sensitive assays detected IL-4, IL-13, IL-31 and TSLP in AEW-treated skin, with TSLP levels significantly increased.</div></div><div><h3>Conclusion</h3><div>Type 2 cytokine-JAK1 signaling is involved in the development of m-alloknesis in dry skin.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"117 3","pages":"Pages 52-60"},"PeriodicalIF":4.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142775917","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":"Melatonin mitigates UV-induced tumorigenesis and suppresses hearing function deterioration in Xpa-deficient mice","authors":"Mariko Tsujimoto ,&nbsp;Takeshi Fujita ,&nbsp;Tatsuya Furukawa ,&nbsp;Yaeno Arima ,&nbsp;Ken-Ichi Nibu ,&nbsp;Chikako Nishigori","doi":"10.1016/j.jdermsci.2025.01.003","DOIUrl":"10.1016/j.jdermsci.2025.01.003","url":null,"abstract":"<div><h3>Background</h3><div>Xeroderma pigmentosum (XP) is caused by impaired DNA repair of UV-induced dipyrimidine-photoproducts. XP cells also show impaired repair/removal of ROS or oxidative DNA lesions caused by UV or 4-nitroquinolline 1-oxide (4NQO). Gene profiling indicated that inflammatory response-related genes are significantly upregulated after UV exposure in XP-A model mice.</div></div><div><h3>Objective</h3><div>Since XP cells are in the state of oxidative stress and inflammation, we aimed to search for therapeutic agents from anti-oxidants/anti-inflammatory drugs, that potentially improve XP symptoms.</div></div><div><h3>Methods</h3><div>Several antioxidants were examined for reducing 4NQO-induced oxidative cytotoxicity or UV-induced oxidative DNA damage in XP-A cells. Among them, we focused on melatonin and evaluated its improving effect for <em>Xpa</em>-deficient MEF on UV-induced cytotoxicity and ROS production, and for <em>Xpa-</em>deficient mice on UV-induced skin tumorigenesis and auditory brainstem responses as one of the neurological symptoms.</div></div><div><h3>Results</h3><div>Melatonin and nicotinamide attenuated 4NQO-induced oxidative cytotoxicity. UV-induced intracellular ROS production and cytotoxicity were improved by melatonin for <em>Xpa</em>-deficient MEF. Finally, the administration of melatonin mitigated UV-induced skin inflammation and tumorigenesis and suppressed hearing deterioration in <em>Xpa</em>-deficient mice.</div></div><div><h3>Conclusion</h3><div>Our results show that melatonin could alleviate XP symptoms through its anti-inflammatory and antioxidant properties.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"117 3","pages":"Pages 81-87"},"PeriodicalIF":4.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143076759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editor's choice","authors":"","doi":"10.1016/S0923-1811(25)00033-7","DOIUrl":"10.1016/S0923-1811(25)00033-7","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"117 3","pages":"Page ii"},"PeriodicalIF":4.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143627868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role and mechanism of JAK2 inhibitor in endothelial mesenchymal transition in systemic sclerosis","authors":"Qingyan Luo ,&nbsp;Xiaoheng Wang ,&nbsp;Yanling Zhang ,&nbsp;Wenrong Xie ,&nbsp;Lina Liang ,&nbsp;Yingping Xu ,&nbsp;Yunshen Liang ,&nbsp;Suyun Ji","doi":"10.1016/j.jdermsci.2025.02.001","DOIUrl":"10.1016/j.jdermsci.2025.02.001","url":null,"abstract":"<div><h3>Background</h3><div>Systemic sclerosis (SSc) is an autoimmune disease characterized by vascular endothelial dysfunction and damage, immune dysregulation and fibrosis. Endothelial mesenchymal transition (EndoMT) has been implicated in the skin fibrosis of SSc. Many studies have demonstrated that janus kinase type2 (JAK2) inhibitor can alleviate skin fibrosis in both SSc patients and bleomycin (BLM)-induced mouse models of SSc. However, the potential therapeutic effect of JAK2 inhibitor on EndoMT in SSc skin, along with the underlying molecular mechanisms, remains unexplored.</div></div><div><h3>Objective</h3><div>To investigate the effects of JAK2 inhibitor on the EndoMT in SSc skin and to elucidate the associated molecular mechanisms.</div></div><div><h3>Methods</h3><div>Wild-type female C57BL/6 mice were divided into several groups to assess the effects of JAK2 inhibitor on EndoMT through H&amp;E staining, masson staining, immunofluorescence and single-cell RNA-sequencing (scRNA-seq). Cultured human umbilical vein endothelial cells (HUVECs) were used to explore the mechanism of action of JAK2 inhibitor on EndoMT using immunofluorescence, quantitative RT-PCR, RNA sequencing and western blot.</div></div><div><h3>Results</h3><div>JAK2 inhibition improved skin fibrosis, reduced CD31/α-SMA co-localisation and the number of EndoMT-activated vascular endothelial cells in bleomycin-induced SSc mice. Treatment of HUVECs with TGF-β or BLM led to a myofibroblast-like morphology and markers, along with downregulation of endothelial cell features, which were reversed following JAK2 inhibition. The activation of the PI3K/Akt/mTOR pathway was involved in EndoMT in HUVECs induced by TGF-β/BLM, and this activation was attenuated by JAK2 inhibition.</div></div><div><h3>Conclusions</h3><div>JAK2 inhibitor may serve as an effective treatment for EndoMT in SSc, potentially through modulation of the PI3K/Akt/mTOR signaling pathway.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"117 3","pages":"Pages 71-80"},"PeriodicalIF":4.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143538268","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, Patryk Porebski, Katharina Klara Hahn, Kexin Liao, Anja Uhmann, Andrea Braun, Prasad Dasari, Michael Peter Schön, Timo Buhl","doi":"10.1016/j.jdermsci.2025.02.007","DOIUrl":"https://doi.org/10.1016/j.jdermsci.2025.02.007","url":null,"abstract":"<p><strong>Background: </strong>Triclosan, a common antimicrobial agent, is widely used in personal-care products and as a topical antiseptic in atopic dermatitis (AD).</p><p><strong>Objective: </strong>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).</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>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.</p>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-02-28","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}