Journal of dermatological science最新文献

{"title":"Single-cell RNA sequencing identifies long non-coding RNAs enriched in psoriatic epidermal subsets","authors":"Longlong Luo ,&nbsp;Jan Cedric Freisenhausen ,&nbsp;Devin Malitha Dompage ,&nbsp;Huaitao Cheng ,&nbsp;Martin Enge ,&nbsp;Andor Pivarcsi ,&nbsp;Enikö Sonkoly","doi":"10.1016/j.jdermsci.2026.03.002","DOIUrl":"10.1016/j.jdermsci.2026.03.002","url":null,"abstract":"<div><h3>Background</h3><div>Psoriasis is a chronic inflammatory skin disease characterised by disrupted crosstalk between keratinocytes and immune cells, resulting in epidermal dysfunction. Long non-coding RNAs (lncRNAs) regulate gene expression in a cell- or tissue-specific manner, yet their role in psoriatic epidermal dysfunction remains poorly understood.</div></div><div><h3>Objectives</h3><div>To generate a single-cell atlas of lncRNA expression in healthy and psoriatic epidermis and identify cell state-specific lncRNAs associated with disease.</div></div><div><h3>Methods</h3><div>Data from Smart-seq2 single-cell RNA sequencing of sorted CD45⁺ and CD45⁻ epidermal cells from healthy controls and lesional/non-lesional psoriatic skin were analysed. Selected lncRNAs were validated by RT-qPCR, single-molecule <em>in situ</em> hybridisation (RNAscope), and immunofluorescence. The regulation of <em>LINC01137</em> was studied in IL-17A-treated primary keratinocytes and 3D epidermal models, and its function assessed using siRNA-mediated knockdown in keratinocytes.</div></div><div><h3>Results</h3><div>We identified 1412 epidermal lncRNAs with robust expression across distinct keratinocyte and immune cell states. LncRNAs exhibited strong cell type-specific expression in both keratinocytes and immune cells, moreover, several lncRNAs showed selective expression in psoriasis-associated cell states. <em>LINC01137</em> was enriched in activated keratinocytes, induced by IL-17A and correlated with TGF-β pathway activity; its knockdown in primary keratinocytes attenuated TGF-β-induced SERPINE1/PAI-1 expression. <em>LINC00892</em> was enriched in lesional Th1, Th17 and proliferating CD8⁺ T cells and showed increased expression as well as co-localisation with the T cell marker CD3 in psoriasis epidermis.</div></div><div><h3>Conclusions</h3><div>This study identifies the single-cell non-coding transcriptomic landscape of the psoriatic epidermis and highlights distinct lncRNA signatures in keratinocytes and immune cells, suggesting their involvement in pathogenic processes in psoriasis.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"122 2","pages":"Pages 36-46"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147577358","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 novel ZIC1–BMP4 axis identified in photoaged dermal fibroblasts regulates melanogenesis","authors":"Mengting Ouyang ,&nbsp;Feng Zhou ,&nbsp;Lei Wen ,&nbsp;Shen Lin ,&nbsp;Amin Yao ,&nbsp;Yu Zhang ,&nbsp;Congxiu Ye ,&nbsp;Qingfang Xu ,&nbsp;Wei Lai","doi":"10.1016/j.jdermsci.2026.03.003","DOIUrl":"10.1016/j.jdermsci.2026.03.003","url":null,"abstract":"<div><h3>Background</h3><div>Chronic ultraviolet exposure induces photoaging and pigmentation, contributing to disorders such as melasma. However, treatments for photoaging-related pigmentation still challenging, implying upstream regulators remain incompletely understood.</div></div><div><h3>Objectives</h3><div>To identify the key regulators involved in photoaging-related pigmentation.</div></div><div><h3>Methods</h3><div>We integrated bulk RNA-seq data of sun-exposed and sun-protected human skin from GTEx dataset and validated with public single-cell RNA-seq data. More than 19,000 genes were screened for correlation with MITF, the key regulator of melanogenesis. Cell states and interactions were further characterized using pySCENIC, pseudotime trajectory analysis, and CellChat. Experimental analyses, including immunohistochemistry, immunofluorescence, ChIP-PCR, and ex vivo human skin culture, were performed to further characterize the biological relevance of the transcriptomic findings.</div></div><div><h3>Results</h3><div>ZIC1 was identified as a fibroblast-specific transcription factor upregulated in photoaged skin and strongly correlated with MITF. It was enriched in fibroblast subsets associated with inflammation and extracellular matrix remodeling, which displayed enhanced BMP4 signaling to melanocytes. Immunostaining confirmed ZIC1 upregulation in sun-exposed and melasma skin, with colocalization in vimentin-positive fibroblasts. Repeated UVA exposure upregulated both ZIC1 and BMP4 in dermal fibroblasts. Gain- and loss-of-function studies, combined with in silico analysis and ChIP-PCR assay, support a positive regulatory link between ZIC1 and BMP4 during photoaging.</div></div><div><h3>Conclusions</h3><div>Our transcriptomic analyses together with preliminary experimental verification suggest a previously unrecognized ZIC-BMP4 axis through which dermal fibroblasts implicated in melanogenesis in photoaged skin, providing new insights into dermal-epidermal crosstalk and highlighting a potential therapeutic target.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"122 2","pages":"Pages 55-65"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147494893","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":"Parbendazole induces semaphorin 3A expression via JNK/c-Jun signaling pathway in normal human epidermal keratinocytes","authors":"Mirei Fujita ,&nbsp;Yayoi Kamata ,&nbsp;Nanami Tanemoto ,&nbsp;Motoki Morita ,&nbsp;Tomohiro Tobita ,&nbsp;Qiaofeng Zhao ,&nbsp;Mitsutoshi Tominaga ,&nbsp;Kenji Takamori","doi":"10.1016/j.jdermsci.2025.12.001","DOIUrl":"10.1016/j.jdermsci.2025.12.001","url":null,"abstract":"<div><h3>Background</h3><div>Epidermal hyperinnervation is a partial cause of antihistamine-resistant itch. The nerve repulsion factor semaphorin 3 A (Sema3A) plays a key role in regulating intraepidermal nerve fiber density. In a preliminary study, we screened pre-existing drugs for potential Sema3A inducers and identified benzimidazole anthelmintics as Sema3A inducers in normal human epidermal keratinocytes (NHEKs).</div></div><div><h3>Objective</h3><div>This study aimed to investigate the mechanisms underlying Sema3A induction by benzimidazole anthelmintics, such as parbendazole, in NHEKs.</div></div><div><h3>Methods</h3><div>Parbendazole was added to NHEKs or a reconstructed human epidermis (RHE) model and incubated for 24 h at 37°C. Sema3A expression levels were analyzed by quantitative real-time PCR and enzyme-linked immunosorbent assay. Cell viability was assessed using a cell-counting kit-8 assay or methylthiazole tetrazolium assay. The molecular mechanisms of Sema3A induction by parbendazole were examined using signaling inhibitors and siRNAs. Phosphorylation of Jun-N-terminal kinase (JNK) and c-Jun was analyzed by western blotting.</div></div><div><h3>Results</h3><div>Parbendazole dose-dependently increased <em>Sema3A</em> gene expression and extracellular secretion in NHEKs, with similar results observed in RHE models. Parbendazole also upregulated the expression of the nerve repulsion factor <em>KAL-1</em> mRNA. Regarding nerve elongation factors, parbendazole decreased nerve growth factor levels, whereas amphiregulin and artemin remained unchanged. Parbendazole promoted JNK and c-Jun phosphorylation in NHEKs. JNK inhibitors suppressed parbendazole-mediated <em>Sema3A</em> induction. Additionally, siRNA targeting c-Jun and the AP-1 inhibitor T-5224 both suppressed parbendazole-induced Sema3A upregulation.</div></div><div><h3>Conclusion</h3><div>Parbendazole dose-dependently induced Sema3A expression via the JNK/c-Jun signaling axis. Benzimidazole anthelmintics may have potential for developing new antipruritic drugs.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"122 2","pages":"Pages 47-54"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147489085","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":"Shiseido Award 2026 announcement","authors":"","doi":"10.1016/S0923-1811(26)00086-1","DOIUrl":"10.1016/S0923-1811(26)00086-1","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"122 2","pages":"Page 70"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147827170","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":"High-throughput sequencing of T-cell receptor beta reveals race and ethnic disparities in cutaneous T-cell lymphoma","authors":"Liliana Crisan ,&nbsp;Lu Chen ,&nbsp;Michelle Afkhami ,&nbsp;Steven T. Rosen ,&nbsp;Raju Pillai ,&nbsp;Christiane Querfeld","doi":"10.1016/j.jdermsci.2026.02.003","DOIUrl":"10.1016/j.jdermsci.2026.02.003","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"122 1","pages":"Pages 23-25"},"PeriodicalIF":4.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147461546","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":"Hsa-microRNA-34a-5p inhibits virus-negative Merkel cell carcinoma cell proliferation and migration by regulating cell cycle- and EMT-related pathways and suppresses tumor spheroid formation","authors":"Giada Badiale ,&nbsp;Christian Felice Cervellera ,&nbsp;Giulia Tonnini ,&nbsp;Agnese Pellati ,&nbsp;Maria Grazia Romanelli ,&nbsp;Andrea Corsi ,&nbsp;Angela Valentino ,&nbsp;Alberto Righi ,&nbsp;Marco Gambarotti ,&nbsp;Antoine Touzé ,&nbsp;Mahtab Samimi ,&nbsp;Aurélie Drouin ,&nbsp;Mauro Tognon ,&nbsp;Chiara Mazziotta ,&nbsp;Fernanda Martini ,&nbsp;John Charles Rotondo","doi":"10.1016/j.jdermsci.2026.02.002","DOIUrl":"10.1016/j.jdermsci.2026.02.002","url":null,"abstract":"<div><h3>Background</h3><div>The molecular mechanisms of Merkel cell polyomavirus (MCPyV)-negative MCC (VN-MCC) initiation remain poorly understood. Although hsa-miR-34a-5p dysregulation has been reported in MCC, its role in VN-MCC is unknown.</div></div><div><h3>Objective</h3><div>We aimed to investigate the functional role of hsa-miR-34a-5p on the malignant phenotype of VN-MCC and elucidate the potential underlying mechanisms.</div></div><div><h3>Methods</h3><div>Hsa-miR-34a-5p expression was investigated in MCC cell lines (n = 5) and tissues (n = 34), and in fibroblast/epithelial cell lines (n = 2). Functional experiments evaluated the effect of hsa-miR-34a-5p on VN-MCC MCC13 phenotype. Gene expression profiling, enrichment analyses and protein–protein interaction network of hsa-miR-34a-5p target genes (n = 84) were conducted in these cells to identify relevant targets/pathways. The impact of hsa-miR-34a-5p on VN-MCC spheroid volume/growth was investigated.</div></div><div><h3>Results</h3><div>Hsa-miR-34a-5p was significantly downregulated in VN-MCC cells and tissues compared to MCPyV-positive counterparts, as well as to fibroblast/epithelial cells. Mechanistically, ectopic hsa-miR-34a-5p expression in MCC13 cells significantly inhibited proliferation, colony formation, and migration abilities, while promoted apoptosis. Hsa-miR-34a-5p silencing in epithelial HaCaT cells increased colony formation and partially enhanced migration. Ectopic hsa-miR-34a-5p expression in MCC13 cells negatively regulated key target genes and pathways involved in both G1/S transition of the cell cycle (<em>CDK4</em>, <em>CDK6</em>, <em>CCNE2</em>) and epithelial-to-mesenchymal transition (<em>MET</em>, <em>NOTCH1</em>, <em>JAG1</em>, along with Snail protein), leading to anti-proliferative and anti-migratory effects. Ectopic hsa-miR-34a-5p expression strongly inhibited MCC13 spheroid formation, whereas miRNA inhibition yielded the opposite effect in HaCaT spheroids from intermediate through later time points.</div></div><div><h3>Conclusion</h3><div>We provide the first functional evidence of the pleiotropic tumor suppressor role of hsa-miR-34a-5p in VN-MCC.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"122 1","pages":"Pages 9-18"},"PeriodicalIF":4.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147446600","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":"Characterization of a unique pathogenic variant in the SERPING1 gene of a patient with hereditary angioedema type I","authors":"Takafumi Hisamoto,&nbsp;Kenta Sentoku,&nbsp;Yutaka Shimomura","doi":"10.1016/j.jdermsci.2026.03.005","DOIUrl":"10.1016/j.jdermsci.2026.03.005","url":null,"abstract":"<div><h3>Background</h3><div>Hereditary angioedema (HAE) is a rare genetic disease characterized by sudden onset of edema involving various organs. Among the three subtypes of the disease, HAE types I and II are caused by heterozygous variants in <em>SERPING1</em> gene encoding C1 inhibitor (C1INH). The pathogenicity of each variant, however, has not fully been revealed.</div></div><div><h3>Objective</h3><div>To assess the mechanism how a <em>SERPING1</em> gene-variant identified in a patient with HAE type I caused the disease.</div></div><div><h3>Methods</h3><div>Genetic analysis was conducted for a Japanese patient with HAE type I. The consequences resulting from the <em>SERPING1</em> gene-variant were analyzed at mRNA levels. Overexpression studies in cultured cells were performed to analyze behavior of the mutant C1INH proteins. Effect of a small interfering RNA specific to the mutant <em>SERPING1</em>-mRNA on expression of wild-type C1INH was also tested.</div></div><div><h3>Results</h3><div>We identified a recurrent heterozygous variant c.820 A&gt;G (p.Ile274Val) in the patient’s <em>SERPING1</em> gene. While we did not find any abnormalities in C1INH with the p.Ile274Val-variant, we found that the variant c.820 A&gt;G caused an aberrant splicing event leading to a frameshift and a premature termination codon. This truncated protein clearly showed a dominant-negative effect against the wild-type C1INH. Finally, we showed that knock-down of the mutant <em>SERPING1</em>-mRNA recovered expression of the wild-type C1INH.</div></div><div><h3>Conclusion</h3><div>A unique pathogenic mechanism for the <em>SERPING1</em> gene-variant c.820 A&gt;G has been disclosed. Furthermore, our findings have raised the possibility that RNA interference could be a new therapeutic tool for the disease.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"122 1","pages":"Pages 1-8"},"PeriodicalIF":4.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147482888","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":"Elevated serum d-ROMs and lesional 4-HNE expression indicate oxidative stress in pemphigus","authors":"Chisato Tawada ,&nbsp;Ryota Asahina ,&nbsp;Yoko Ueda ,&nbsp;Xiaoyu Zang ,&nbsp;Kayoko Tanaka ,&nbsp;Hiromu Tsuji ,&nbsp;Hirofumi Niwa ,&nbsp;Tomoyuki Hioki ,&nbsp;Hiroaki Iwata","doi":"10.1016/j.jdermsci.2026.03.006","DOIUrl":"10.1016/j.jdermsci.2026.03.006","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"122 1","pages":"Pages 19-22"},"PeriodicalIF":4.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147482839","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":"Comprehensive analysis of tonsillar gene expression and the tonsillar microbiota in patients with palmoplantar pustulosis and pustulotic arthro-osteitis","authors":"Satomi Kobayashi ,&nbsp;Hideki Nakagawa ,&nbsp;Masato Komai","doi":"10.1016/j.jdermsci.2026.01.006","DOIUrl":"10.1016/j.jdermsci.2026.01.006","url":null,"abstract":"<div><h3>Background</h3><div>Tonsillectomy improves symptoms in patients with palmoplantar pustulosis (PPP) and suppresses disease progression in patients with pustulotic arthro-osteitis (PAO), highlighting the important role of tonsils in the pathogenesis of PPP/PAO.</div></div><div><h3>Objective</h3><div>To identify inflammatory pathways involved in the tonsil tissue of patients with PPP/PAO, and to clarify the characteristics of tonsillar microbiota.</div></div><div><h3>Methods</h3><div>We assessed gene expression in tonsil tissue obtained from PPP/PAO or recurrent tonsillitis (RT)/sleep apnea syndrome (SAS) patients using microarray and quantitative reverse transcription polymerase chain reaction analysis. We also performed a comprehensive analysis of the tonsillar microbiota using next-generation sequencing. Potential associations between tonsillar gene expression and bacterial composition or disease activities were evaluated.</div></div><div><h3>Results</h3><div>Twenty-five tonsils from PPP/PAO patients and 15 tonsils from RT/SAS patients were included. The gene expression of inflammatory cytokines and molecules involved in the Th17, Th2, and Treg pathways was significantly higher in PPP/PAO tonsils than in RT/SAS tonsils. A significant positive correlation between <em>Streptococcus</em> spp. and the expression of Th17 and Th2 pathway genes was revealed both in PPP/PAO and RT/SAS, however, different correlation patterns were observed between these groups for the other genera. PAO disease activity showed a negative correlation with the expression of <em>CCR4</em>, <em>FOXP3</em>, and <em>CXCR3</em> genes.</div></div><div><h3>Conclusion</h3><div>PPP/PAO tonsils exhibit enhanced Th17, Th2, and Treg responses relative to RT/SAS, indicating a complex inflammatory condition. <em>Streptococcus</em> genus may be associated with inflammation, and interaction between microbiota and T cell immunity would be suggested in PPP/PAO tonsils. PAO disease activity inversely correlated with Treg response.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"121 3","pages":"Pages 12-21"},"PeriodicalIF":4.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147367660","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":"VEGFR-2-targeted photoimmunotherapy for psoriasis-like plaques in a mouse model","authors":"Minako Ogawa-Tominaga ,&nbsp;Yozo Ishiuji ,&nbsp;Takashi Nishimura ,&nbsp;Makoto Mitsunaga ,&nbsp;Masayuki Saruta ,&nbsp;Yoshimasa Nobeyama ,&nbsp;Akihiko Asahina","doi":"10.1016/j.jdermsci.2026.01.004","DOIUrl":"10.1016/j.jdermsci.2026.01.004","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"121 3","pages":"Pages 32-35"},"PeriodicalIF":4.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146168593","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}