Journal of dermatological science最新文献

{"title":"Heparinoid and phospho-pyridoxal preserve tight junction integrity in human skin under oxidative stress","authors":"Hiroki Sakamoto , Ryota Asahina , Momoyo Nishikawa , Seigo Yamada , Gyohei Egawa , Kenji Kabashima","doi":"10.1016/j.jdermsci.2026.03.007","DOIUrl":"10.1016/j.jdermsci.2026.03.007","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"122 2","pages":"Pages 66-69"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147597209","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(26)00090-3","DOIUrl":"10.1016/S0923-1811(26)00090-3","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"122 2","pages":"Page ii"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147827172","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":"Inhibition of eukaryotic translation initiation factor 1 A (eIF1A) and 3B (eIF3B) diminishes the psoriatic phenotype in two mouse models and human 3D model samples","authors":"Nicole Golob-Schwarzl ,&nbsp;Natalie Bordag ,&nbsp;Nitesh Shirsath ,&nbsp;Christin-Therese Müller ,&nbsp;Amin El-Heliebi ,&nbsp;Peter Wolf","doi":"10.1016/j.jdermsci.2026.03.008","DOIUrl":"10.1016/j.jdermsci.2026.03.008","url":null,"abstract":"<div><h3>Background</h3><div>Psoriasis is a systemic inflammatory skin disease for which new topical treatments are needed. Psoriatic inflammation is associated with overexpression of eukaryotic translation initiation factors (eIFs), which regulate gene expression in processes such as proliferation, apoptosis, and differentiation. However, their role in psoriasis remains unclear.</div></div><div><h3>Objective</h3><div>To investigate the contribution of eIF1A and eIF3B to psoriasis pathogenesis and evaluate the therapeutic potential of their inhibition via small interfering RNA (siRNA).</div></div><div><h3>Methods</h3><div>We used two mouse models reflecting different mechanisms of psoriasis: (i) topical application of imiquimod (IMQ) and (ii) K5.TGFβ transgenic mice promoting keratinocyte proliferation. eIF1A and eIF3B were inhibited by either topical or systemic siRNA administration. A 3D human psoriasis model was also used for validation.</div></div><div><h3>Results</h3><div>Inhibition of eIF1A and eIF3B reduced inflammation in both mouse models and the 3D human model. Downregulation of these factors normalized keratinocyte proliferation, epidermal thickness, and cytokine expression (e.g., TNFα, IL-1β, IL-17, IL-22). Differentiation markers such as KRT16 and FLG were restored. These findings suggest that eIF1A and eIF3B play a key role in maintaining the psoriatic inflammatory phenotype.</div></div><div><h3>Conclusion</h3><div>Our findings reveal a translational imbalance in psoriasis and identify eIF1A and eIF3B as crucial regulators of disease pathophysiology. Targeting these factors represents a promising new therapeutic strategy for psoriasis treatment.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"122 2","pages":"Pages 27-35"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147597279","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":"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":"Epidermal deletion of Kindlin-1 drives matrix changes in the mouse skin and altered responses to ultraviolet radiation.","authors":"Giovana Carrasco, Emily R Webb, Molly R Danks, Morwenna Muir, David Hardman, Chinmayi Pednekar, Roza H A Masalmeh, Martin Lee, Rashi Krishna, Alex von Kriegsheim, Miguel O Bernabeu, Albena T Dinkova-Kostova, Valerie G Brunton","doi":"10.1016/j.jdermsci.2026.04.007","DOIUrl":"https://doi.org/10.1016/j.jdermsci.2026.04.007","url":null,"abstract":"<p><strong>Background: </strong>Kindler syndrome (KS) or Kindler epidermolysis bullosa (KEB) is a rare genetic autosomal skin fragility disorder with photosensitivity and abnormal pigmentation, with patients also having an increased risk of developing cutaneous squamous cell carcinoma (cSCC).</p><p><strong>Objective: </strong>Gain a better understanding of the pathophysiology of KEB and the effects of UV radiation.</p><p><strong>Methods: </strong>We generated a K14CreER^T2 Kindlin-1^-/- SKH1 mouse which provides a valuable model to understand the complex interactions between keratinocytes and the skin environment following epidermal deletion of Kindlin-1 in adult mice.</p><p><strong>Results: </strong>Proteomic analysis of mouse skin identified significant changes associated with an epithelial-to-mesenchymal transition (EMT) including the upregulation of several extracellular matrix (ECM) proteins comprising fibrillar collagens and matrix remodeling enzymes following deletion of Kindlin-1. Detailed analysis of collagen within the skin showed increased content and fiber alignment consistent with a more fibrotic environment. Mechanistically, we found increased TGFβ signaling and activation of dermal fibroblasts in Kindlin-1 deleted skin, highlighting the importance of paracrine signaling in the control of skin homeostasis by Kindlin-1. Kindlin-1 deletion led to profound suppression of gene expression of the antioxidant enzyme Gstp1 and exacerbated ultraviolet radiation (UVR) induced DNA damage consistent with increased TGFβ signaling and an inability of Kindlin-1 deleted skin to mount an effective protective response to UVR.</p><p><strong>Conclusion: </strong>This work offers insights into how Kindlin-1 loss alters skin homeostasis and induces a tumor-permissive environment.</p>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147847989","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":"Modulation of proinflammatory but not regulatory cytokines by in vitro JAK inhibition in peripheral blood B-cells of patients with psoriatic arthritis.","authors":"Antonio Tonutti, Natasa Isailovic, Francesca Motta, Rita Ragusa, Giacomo M Guidelli, Nicoletta Luciano, Angela Ceribelli, Carlo Selmi, Maria De Santis","doi":"10.1016/j.jdermsci.2026.04.009","DOIUrl":"https://doi.org/10.1016/j.jdermsci.2026.04.009","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848032","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":"Treg cells as potential therapeutic targets for bullous pemphigoid: A review.","authors":"Honghao He, Shiguang Peng, Xinyi Wei, Jinqing Zhang, Mei Cao, Fang Liu, Rina Su","doi":"10.1016/j.jdermsci.2026.04.003","DOIUrl":"https://doi.org/10.1016/j.jdermsci.2026.04.003","url":null,"abstract":"<p><p>Bullous pemphigoid (BP) is an autoimmune disease characterized by Bullous pemphigoid antigen 180(BP180) and Bullous pemphigoid antigen 230(BP230) autoantibodies production. Regulatory T cells (Tregs) are key cells for the maintenance of immune tolerance. Increasing evidence suggests that Treg dysfunction leads to autoantibody production and skin rashes in mice and humans, making immunomodulatory therapies targeting Tregs a potential therapeutic strategy for BP. Low-dose Interleukin-2 treatment and adoptive cell therapy are promising methods to modulate Tregs' numbers and function. Herein, we review the immunological mechanisms underlying BP pathogenesis, with an emphasis on the protective role of Treg cell-mediated immune tolerance in BP. Furthermore, we explore the potential therapeutic applications of Treg-based therapies for BP, providing novel insights into patient management.</p>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147793156","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}