Journal of dermatological science最新文献

{"title":"Low-temperature plasma-activated Ringer’s lactate solution induces apoptosis in melanoma cells by downregulating heat shock proteins and by inducing mitochondrial dysfunction","authors":"Akira Miyazaki ,&nbsp;Tomoki Taki ,&nbsp;Kae Nakamura ,&nbsp;Mariko Ogawa-Momohara ,&nbsp;Hiromasa Tanaka ,&nbsp;Masaru Hori ,&nbsp;Katsumi Ebisawa ,&nbsp;Masashi Akiyama","doi":"10.1016/j.jdermsci.2026.01.003","DOIUrl":"10.1016/j.jdermsci.2026.01.003","url":null,"abstract":"<div><h3>Background</h3><div>Low-temperature plasma (LTP) is an essential technology in engineering that originated in materials science. Its applications have recently been expanded to biology, where it is referred to as plasma biology. LTP and LTP-activated solutions are now used for wound healing and sterilization. One emerging field is cancer treatment.</div></div><div><h3>Objective</h3><div>To evaluate the effectiveness of LTP-activated Ringer’s lactate solution (PAL) against malignant melanoma.</div></div><div><h3>Methods</h3><div>Cells of the A375 malignant melanoma line were subcutaneously injected into nude mice. PAL was administered three times weekly, and tumor growth was measured. Cell viability was measured using MTS assay <em>in vitro</em> experiments. Whole transcriptome sequencing and qRT-PCR were conducted to reveal differentially expressed mRNAs. To detect DNA double-strand breaks, immunofluorescence of γ-H2AX foci was performed. Mitochondrial membrane potential and apoptosis were detected by JC-1 probe and caspase-3/7 detection reagents, respectively.</div></div><div><h3>Results</h3><div>The PAL exhibited an anti-cancer effect in the A375 xenograft mouse model. The PAL also showed <em>in vitro</em> cytotoxicity for a melanoma cell line<em>.</em> Comprehensive RNA expression analysis revealed the downregulation of multiple heat shock proteins (HSPs), especially HSPA1A, HSPA1B, HSPA6, HSPA7 and DNAJB1. HSP insufficiency induced lower mitochondrial membrane potential. The mode of cell death for the melanoma cells was apoptosis.</div></div><div><h3>Conclusion</h3><div>PAL is suggested as a promising new therapeutic agent for malignant melanoma.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"121 2","pages":"Pages 48-55"},"PeriodicalIF":4.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146088693","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":"Erratum to “Transcriptional regulation of Mlph and Rab27a by PAX3-NF-κB interaction in melanosome transport of melanocytes” [J. Dermatol. Sci. 120 (2025) 98–104]","authors":"HaiRu Zhao ,&nbsp;SeongWon Park ,&nbsp;ChanSong Jo,&nbsp;JeongMi Lee,&nbsp;JaeSung Hwang","doi":"10.1016/j.jdermsci.2025.12.005","DOIUrl":"10.1016/j.jdermsci.2025.12.005","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"121 1","pages":"Page 26"},"PeriodicalIF":4.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145949171","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":"SMYD2 promotes oxidative stress-responsive lipid metabolism in melanoma by regulating H3K4 tri-methylation","authors":"Bing Han ,&nbsp;Henan Si ,&nbsp;Shuyue Yang ,&nbsp;Zhiyang Huang ,&nbsp;Shanshan Li ,&nbsp;Hesong Liu ,&nbsp;Mengdi Zhang ,&nbsp;Lei Yao","doi":"10.1016/j.jdermsci.2025.12.004","DOIUrl":"10.1016/j.jdermsci.2025.12.004","url":null,"abstract":"<div><h3>Background</h3><div>Lipid metabolism is increasingly recognized as a critical role in cancer biology, influencing membrane dynamics, energy homeostasis, and cell survival. In melanoma, the specific regulatory mechanisms linking lipid metabolism and tumor progression remain poorly understood. Epigenetic modifiers have emerged as key regulators in metabolic reprogramming and tumor progression.</div></div><div><h3>Objective</h3><div>To investigate the role of SMYD2, a histone methyltransferase, in the regulation of lipid metabolism and oxidative stress in melanoma.</div></div><div><h3>Methods</h3><div>SMYD2 levels in melanoma tissues were analyzed in relation to patient prognosis. SMYD2 knockdown was achieved via shRNA in melanoma cell lines, followed by assays for proliferation, migration, and apoptosis. ChIP-qPCR was used to assess SMYD2-mediated trimethylation of H3K4 (H3K4me3) at the promoter regions of superoxide dismutase 1 (SOD1) and glutathione peroxidase 1 (GPX1). Fatty acid levels and markers of oxidative stress were measured using biochemical assays and western blot.</div></div><div><h3>Results</h3><div>Elevated SMYD2 expression was correlated with poor prognosis in melanoma patients. SMYD2 knockdown significantly inhibited melanoma cell proliferation and migration while inducing apoptosis. Mechanistically, SMYD2 directly facilitated H3K4me3 at the promoters of SOD1 and GPX1, enhancing their transcription. The upregulation of SOD1 and GPX1 reduced oxidative stress levels and, in turn, promoted fatty acid synthesis and lipid accumulation.</div></div><div><h3>Conclusion</h3><div>SMYD2 functions as an oncogene in melanoma by epigenetically upregulating antioxidant genes SOD1 and GPX1, thereby alleviating oxidative stress and driving lipid reprogramming. These findings uncover a novel SMYD2–oxidative stress–lipid metabolism axis and highlight SMYD2 as a potential therapeutic target in melanoma.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"121 1","pages":"Pages 11-21"},"PeriodicalIF":4.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145949165","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":"Cyclin E1 is dispensable for skin homeostasis and hyperplasia but is essential for carcinogenesis","authors":"Lizbeth Contreras ,&nbsp;Ana Marcos-Díaz ,&nbsp;Lorena García-Gaipo ,&nbsp;Berta Casar ,&nbsp;Alberto Gandarillas","doi":"10.1016/j.jdermsci.2025.11.001","DOIUrl":"10.1016/j.jdermsci.2025.11.001","url":null,"abstract":"<div><h3>Background</h3><div>Epidermal renewal needs tight control of the cell cycle and proliferation to face the continuous mutagenic pressure of UV light. Cyclin E1 is a key molecule in human epidermis, a main driver of the cell cycle and is frequently deregulated in cancer. Both Cyclin E1 and the homologue Cyclin E2 were shown generally dispensable for normal development and growth. However, their requirement for skin hyperplasia and squamous carcinogenesis was unknown.</div></div><div><h3>Objective</h3><div>We aimed to investigate the requirement of Cyclin E for skin homeostasis, hyperplasia and carcinogenesis.</div></div><div><h3>Methods</h3><div>We studied the skin and isolated keratinocytes in the absence of Cyclin E1. We analysed steady-state and hyperplastic defective epidermis and monitored carcinogen-induced skin carcinogenesis.</div></div><div><h3>Results</h3><div>Cyclin E1-defective skin displayed normal histology and function. The epidermis displayed no differences in the capacity to boost proliferation after induction of hyperplasia. However, the lack of the cyclin strikingly overrode carcinogen-induced tumourigenesis. The absence of Cyclin E1 was not compensated by a rise of Cyclin A, another CDK2 potential regulator. Instead, Cyclin E2 was up-regulated in steady-state and hyperplastic skin, providing compensatory potential. However, we did not detect Cyclin E2 in most wild type tumours, especially in the less differentiated carcinomas.</div></div><div><h3>Conclusion</h3><div>Contrary to the situation in normal development, the results show that either Cyclin E1 or Cyclin E2 is essential for tumorigenesis. They also suggest that in the absence of Cyclin E1, Cyclin E2 serves homeostasis, whereas the oncogenic pathways suppress this compensation as an anti-tumour, self-preserve mechanism.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"121 1","pages":"Pages 1-10"},"PeriodicalIF":4.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145558527","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":"Adenosine A2A receptors are expressed on the bottom of basal keratinocytes and promote keratinocyte proliferation in human skin","authors":"Kazuki Takagaki,&nbsp;Shinobu Nakanishi","doi":"10.1016/j.jdermsci.2025.11.002","DOIUrl":"10.1016/j.jdermsci.2025.11.002","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"121 1","pages":"Pages 22-25"},"PeriodicalIF":4.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145688906","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":"Transcriptional regulation of Mlph and Rab27a by PAX3-NF-κB interaction in melanosome transport of melanocytes","authors":"HaiRu Zhao ,&nbsp;SeongWon Park ,&nbsp;ChanSong Jo,&nbsp;JeongMi Lee,&nbsp;JaeSung Hwang","doi":"10.1016/j.jdermsci.2025.10.001","DOIUrl":"10.1016/j.jdermsci.2025.10.001","url":null,"abstract":"<div><h3>Background</h3><div>Melanosome transport is a highly coordinated process involving both microtubule- and actin-dependent mechanisms. Our previous study identified 2-methyl-naphtho[1,2,3-de]quinolin-8-one (MNQO) as an inhibitor of melanosome transport. In the present study, we aimed to elucidate the transcriptional regulation of melanosome transport by identifying the key transcription factors involved in this process.</div></div><div><h3>Objective</h3><div>This study investigates the regulation of <em>NF-κB</em> by <em>PAX3</em> and its role in binding to the enhancer regions of <em>Rab27a</em> and <em>Mlph</em> to modulate melanosome transport.</div></div><div><h3>Methods</h3><div>Mouse melanocytes were transfected with Pax3-specific siRNA (si<em>PAX3</em>), followed by the assessment of melanosome aggregation. <em>NF-κB</em> expression was analyzed using Western blot and RT-PCR. Chromatin immunoprecipitation (ChIP) and electrophoretic mobility shift assay (EMSA) were performed to determine NF-κB binding to the enhancer regions of Rab27a and Mlph.</div></div><div><h3>Results</h3><div>Silencing of P<em>AX3</em> significantly impaired melanosome transport, leading to the intracellular accumulation of melanosomes. Moreover, <em>PAX3</em> knockdown markedly decreased the expression levels of <em>Mlph</em> and <em>Rab27a</em>. ChIP and EMSA assays further demonstrated that <em>NF-κB</em> directly binds to the enhancer regions of <em>Rab27a</em> (+51,608 to +51,619 bp relative to the TSS) and <em>Mlph</em> (+34,021 to +34,033 bp relative to the TSS).</div></div><div><h3>Conclusion</h3><div>This study provides the first evidence of a regulatory relationship between <em>PAX3</em> and <em>NF-κB</em>, wherein <em>NF-κB</em> directly binds to the enhancer regions of <em>Rab27a</em> and <em>Mlph</em> to modulate melanosome transport. These findings offer novel insights into the transcriptional control of melanogenesis and its potential implications for melanoma research.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"120 3","pages":"Pages 98-104"},"PeriodicalIF":4.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145369186","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":"Three-dimensional cultured human skin model replicating a human facial shape enables personalized assessment of UVB damage in various facial areas","authors":"Katsuma Miyachi ,&nbsp;Takaaki Yamada ,&nbsp;Takeru Siraishi ,&nbsp;Toshio Igarashi ,&nbsp;Ryosuke Okuno ,&nbsp;Yuichi Hasebe ,&nbsp;Osamu Hirose ,&nbsp;Seiji Hasegawa","doi":"10.1016/j.jdermsci.2025.10.002","DOIUrl":"10.1016/j.jdermsci.2025.10.002","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"120 3","pages":"Pages 105-108"},"PeriodicalIF":4.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145369268","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":"Bead aggregation assays with desmoglein and desmocollin for the evaluation of disease activity in pemphigus","authors":"Miki Hamanaka ,&nbsp;Ken Ishii ,&nbsp;Mari Urushibata ,&nbsp;Kenji Yoshida ,&nbsp;Akira Ishiko","doi":"10.1016/j.jdermsci.2025.10.003","DOIUrl":"10.1016/j.jdermsci.2025.10.003","url":null,"abstract":"<div><h3>Background</h3><div>Previously, we developed bead aggregation assays with recombinant desmoglein (Dsg) and desmocollin (Dsc) and found that pemphigus autoantibodies directly block the heterophilic trans-interaction of Dsg/Dsc.</div></div><div><h3>Objective</h3><div>To investigate whether inhibitory activities measured by bead aggregation assays can be used to assess pemphigus disease activity.</div></div><div><h3>Methods</h3><div>First, we investigated whether the inhibitory activity correlated with patients’ clinical disease activity using sera of 21 pemphigus vulgaris (PV) and 16 pemphigus foliaceus (PF) cases at the time of initial diagnosis. Next, we investigated whether the inhibitory activities reflect disease activities along the time course.</div></div><div><h3>Results</h3><div>The inhibitory activities were significantly correlated with the pemphigus disease area index (PDAI) (Spearman rank correlation, 0.761, n = 21, p &lt; 0.01) in the PV group. However, no significant correlation was observed between Dsg3 ELISA titers and PDAI (Spearman rank correlation, 0.238, p &gt; 0.05). Similar results were observed in the PF group (0.746, p &lt; 0.01 vs. 0.357, p &gt; 0.05). The inhibitory activities were evaluated using sera from the initial onset, remission, and relapse stages for four PV and four PF cases. The inhibitory activity changed in parallel with the clinical disease activity in seven out of eight cases. In two cases, the inhibitory activity correlated more accurately with disease activity than the Dsg ELISA titers.</div></div><div><h3>Conclusions</h3><div>Bead assay is useful for assessing disease activity in patients with pemphigus. Furthermore, our findings suggest that the direct inhibition of Dsg/Dsc adhesion is important for pemphigus pathogenesis.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"120 3","pages":"Pages 88-97"},"PeriodicalIF":4.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145427261","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 reappraisal of type 2 cytokine-producing cells in atopic dermatitis: Spotlight on Tc2 cells","authors":"Tetsuya Honda","doi":"10.1016/j.jdermsci.2025.09.006","DOIUrl":"10.1016/j.jdermsci.2025.09.006","url":null,"abstract":"<div><div>Atopic dermatitis (AD) is a chronic inflammatory skin disorder driven by type 2 cytokines, particularly IL-4, IL-13, and IL-31. CD4⁺ Th2 cells have long been considered the primary producers of these cytokines in AD, but the contribution of CD8⁺ Tc2 cells has received limited attention. Recent advances in single-cell RNA sequencing, which allow for cytokine expression profiling at the single-cell level, challenge this traditional paradigm. This review reappraises the cellular sources of IL-13—a key effector cytokine in AD lesions—by not only summarizing prior studies but also reanalyzing multiple publicly available scRNA-seq datasets. These analyses indicate that Tc2 cells may represent a substantial, and in some cases dominant, source of IL-13 in lesional skin, alongside Th2 cells. This perspective invites a reconsideration of the Th2-centric model and proposes that a broader view—including Tc2 cells—is needed to fully understand type 2 immune responses in AD.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"120 3","pages":"Pages 81-87"},"PeriodicalIF":4.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145277086","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 case of metastatic breast carcinoma to the skin expressing SARS-CoV-2 spike protein possibly derived from mRNA vaccine","authors":"Shigetoshi Sano","doi":"10.1016/j.jdermsci.2025.09.007","DOIUrl":"10.1016/j.jdermsci.2025.09.007","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"120 2","pages":"Pages 71-73"},"PeriodicalIF":4.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145277080","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}