Journal of dermatological science最新文献

{"title":"Eribulin inhibits tumor growth of two novel patient-derived xenograft models of Merkel cell carcinoma","authors":"Kodai Miyamoto ,&nbsp;Teruki Yanagi ,&nbsp;Takuya Maeda ,&nbsp;Shinya Kitamura ,&nbsp;Hiroshi Nishihara ,&nbsp;Ririko Iwamoto ,&nbsp;Kenzo Takahashi ,&nbsp;Hideyuki Ujiie","doi":"10.1016/j.jdermsci.2025.05.007","DOIUrl":"10.1016/j.jdermsci.2025.05.007","url":null,"abstract":"<div><h3>Background</h3><div><span><span>Merkel cell carcinoma (MCC) is a rare, aggressive neuroendocrine skin cancer with a poor prognosis in advanced cases. Despite reported sensitivities to chemotherapy and </span>immunotherapy, response rates remain limited to approximately 50 % of cases. Although developing novel therapeutic strategies against MCC has been desired, few preclinical models, including cell lines and patient-derived </span>xenografts (PDXs), are available.</div></div><div><h3>Objectives</h3><div>This study aimed to establish novel preclinical research models and develop novel therapeutic strategies for MCC.</div></div><div><h3>Methods</h3><div>We analyzed 19 clinical MCC samples in our department. Moreover, to establish novel PDX tumors, we transplanted MCC tissues from Japanese patients into immunodeficient NOD/SCID mice.</div></div><div><h3>Results</h3><div><span>Histopathological analyses of 19 clinical MCC samples in our department revealed the tumors to either be infected with the Merkel cell polyomavirus<span> or have lost the expression of tumor suppressors (tumor protein p53 [p53] or RB transcriptional corepressor 1 [Rb1]). To establish novel PDX tumors, we transplanted MCC tissues from Japanese patients into immunodeficient NOD/SCID mice. Two MCC-PDX tumors were successfully implanted (MCC-PDX-MK1 and -MK2), and their histopathological and genetic characteristics were consistent with those of the original tumor. As in vivo preclinical treatments, we administered cisplatin<span>, etoposide<span>, docetaxel, or </span></span></span></span>eribulin<span> to the NOD/SCID mice. Eribulin showed antitumor activity in both MCC-PDX models.</span></div></div><div><h3>Conclusion</h3><div>Two MCC-PDX models were established successfully, and therapeutic experiments suggest that eribulin could inhibit MCC tumor growth.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"119 2","pages":"Pages 82-89"},"PeriodicalIF":4.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144268247","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":"Long-read sequencing cracks unsolved cases and further improves genome diagnostics in epidermolysis bullosa","authors":"Eddy N. de Boer ,&nbsp;L. Agnes Grutters ,&nbsp;Rosalie Baardman ,&nbsp;Daniëlle Schoonhoven ,&nbsp;Jeroen Bremer ,&nbsp;Rindert R. Venema ,&nbsp;Femke Boorsma ,&nbsp;Jelkje J. de Boer-Bergsma ,&nbsp;Gilles F.H. Diercks ,&nbsp;Henny H. Lemmink ,&nbsp;Sabrina Z. Commandeur-Jan ,&nbsp;Dorieke. J. Dijkstra ,&nbsp;Lennart F. Johansson ,&nbsp;Marieke C. Bolling ,&nbsp;Cleo C. van Diemen ,&nbsp;Peter C. van den Akker","doi":"10.1016/j.jdermsci.2025.04.014","DOIUrl":"10.1016/j.jdermsci.2025.04.014","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"119 2","pages":"Pages 97-100"},"PeriodicalIF":4.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144113152","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)00135-5","DOIUrl":"10.1016/S0923-1811(25)00135-5","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"119 2","pages":"Page ii"},"PeriodicalIF":4.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144867002","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 deep intronic founder variant in the SERPINB7 gene causing aberrant splicing is a potential therapeutic target for Nagashima-type palmoplantar keratoderma","authors":"Yuqi Chen ,&nbsp;Zhiming Chen ,&nbsp;Siyuan Li ,&nbsp;Juan Liu ,&nbsp;Yihe Liu ,&nbsp;Qingyue Fu ,&nbsp;Wenbo Bu ,&nbsp;Shuya Sun ,&nbsp;Tianxiao Li ,&nbsp;Ruiyu Xiang ,&nbsp;Zhongya Song ,&nbsp;Ran Mo ,&nbsp;Yong Yang","doi":"10.1016/j.jdermsci.2025.05.004","DOIUrl":"10.1016/j.jdermsci.2025.05.004","url":null,"abstract":"<div><h3>Background</h3><div><span>Nagashima-type palmoplantar keratoderma (NPPK), caused by biallelic </span><em>SERPINB7</em><span> loss-of-function variants, lacks effective treatments. Intriguingly, monoallelic exonic variants are observed in some patients with NPPK, suggesting additional genetic variants.</span></div></div><div><h3>Objective</h3><div>To characterize a deep intronic <em>SERPINB7</em><span><span> variant’s pathogenicity, elucidate its splicing dysregulation, and evaluate antisense </span>oligonucleotide (ASO) therapy.</span></div></div><div><h3>Methods</h3><div><span><span>A customized next-generation sequencing panel was applied to six Chinese NPPK patients. Pathological changes were analyzed by H&amp;E staining and immunofluorescence. </span>RNA<span> extracted from palmar skin was assessed for splicing alterations. Plasmids were generated to evaluate the expression and function of mutant SERPINB7 protein. Haplotype analysis was conducted to confirm the founder effect. RNA pull-down assays and mass spectrometry<span> were used to identify the key splicing factor. Minigene constructs were developed to characterize the splicing process </span></span></span><em>in vitro</em><span>. Finally, an ASO was designed to target this variant.</span></div></div><div><h3>Results</h3><div>A deep intronic <em>SERPINB7</em> variant was identified in six NPPK patients, leading to pseudo-exon inclusion and the production of a truncated, dysfunctional SERPINB7 protein. Haplotype analysis confirmed it as a Chinese founder variant. RNA pull-down assays revealed excessive SRSF9 binding to the abnormal transcript. <em>In vitro</em>, the ASO successfully corrected the aberrant splicing.</div></div><div><h3>Conclusion</h3><div>This study established the pathogenicity of a deep intronic founder variant in <em>SERPINB7</em> driving NPPK via SRSF9-mediated splicing dysregulation, demonstrating ASO therapeutic potential. Findings provide mechanistic insights and a targeted approach for precision therapy development for NPPK.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"119 2","pages":"Pages 73-81"},"PeriodicalIF":4.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144512866","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":"Healthy skin, Healthy brain","authors":"Kyeong-No Yoon ,&nbsp;Jin Ho Chung","doi":"10.1016/j.jdermsci.2025.06.001","DOIUrl":"10.1016/j.jdermsci.2025.06.001","url":null,"abstract":"<div><div>Skin aging extends beyond aesthetic concerns and is increasingly recognized as a key contributor to brain aging through neuroendocrine, inflammatory, and neurochemical mechanisms. Traditionally considered as a peripheral barrier, the skin is now recognized as a neuroendocrine organ capable of communicating with the central nervous system (CNS) via hormone secretion, cytokine signaling, and neurotransmitter modulation. Recent literature has begun to formalize the concept of the skin–brain axis as a bidirectional communication system, particularly within the contexts of psychodermatology and neuroimmunology. This review highlights how extrinsic factors such as ultraviolet (UV) radiation and intrinsic aging disrupt skin homeostasis and trigger systemic effects on brain functions. Chronic UV exposure activates the cutaneous hypothalamic-pituitary-adrenal (HPA) axis and increases systemic cortisol levels, impairing hippocampal neurogenesis and cognitive function. UV-induced alterations in neurotransmitters including glutamate, dopamine, and β-endorphins affect learning, memory, and emotion regulation. Importantly, both photoaging and natural skin aging are associated with reduced synthesis of brain-derived neurotrophic factor (BDNF) in the skin, potentially diminishing systemic BDNF availability, and contributing to cognitive decline. Recent studies explored the protective effects of sunscreen and moisturizers in mitigating cutaneous inflammation and reducing neurodegenerative risk. Additionally, topical or dietary interventions, such as plant-derived polyphenols, may restore skin BDNF levels and enhance skin-brain resilience. Collectively, these findings support a paradigm shift: preserving skin health is not only a dermatological goal, but also a promising strategy for mitigating brain aging and promoting cognitive resilience.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"119 2","pages":"Pages 47-52"},"PeriodicalIF":4.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144669177","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":"C-C motif chemokine receptor 7 (CCR7) in the spinal cord inhibits chronic itch through the neuropeptide NPY","authors":"Yanying Tan ,&nbsp;Zhongqiu Zhao ,&nbsp;Xue Luo ,&nbsp;Xuebin Han ,&nbsp;Hui Xiong ,&nbsp;Zhinan Mei","doi":"10.1016/j.jdermsci.2025.05.001","DOIUrl":"10.1016/j.jdermsci.2025.05.001","url":null,"abstract":"<div><h3>Background</h3><div><span>Studies showed that C-C motif chemokine receptor 7 (CCR7) contributes to the maintenance of </span>neuropathic pain. However, whether CCR7 is involved in chronic itch remains unclear.</div></div><div><h3>Objective</h3><div>To explore the relationship between CCR7 and chronic itch.</div></div><div><h3>Methods</h3><div><span>The scratching behavior of wild-type (WT) and </span><em>Ccr7</em>^<em>-/-</em><span> mice in acute and chronic itch models, or of WT mice in chronic itch after intrathecal<span> injection of CCR7 neutralizing antibody<span> was compared. Mechanical, thermal, and inflammatory pain responses of </span></span></span><em>Ccr7</em>^<em>-/-</em> mice and WT mice were examined. The expression of CCR7, some known lamina-specific markers, and itch-related mediators in the spinal cord of WT and <em>Ccr7</em>^<em>-/-</em><span><span> mice with chronic itch were detected by immunostaining and qRT-PCR respectively. Finally, to explore the possible relationship between CCR7 and </span>Neuropeptide Y<span> (NPY), intrathecal injection of CCR7-siRNA for </span></span><em>in vivo</em><span> knockdown and neurotoxin bombesin-saporin for GRPR-expressing cells ablation were used.</span></div></div><div><h3>Results</h3><div><em>Ccr7</em>^<em>-/-</em><span> mice displayed increasing scratching in chronic itch models. CCR7 neutralizing antibody elevated, while CCR7 ligands CCL19/CCL21 alleviated the scratching behavior in chronic itch models. However, the responses of </span><em>Ccr7</em>^<em>-/-</em><span> mice to mechanical, thermal, and inflammatory pain did not differ from their WT controls. Also, CCR7</span>⁺<span> interneurons co-express NPY, and CCR7 expression was enhanced in the spinal cord of mice with chronic itch. Furthermore, spinal NPY expression was down-regulated in </span><em>Ccr7</em>^<em>-/-</em><span> mice or after CCR7-siRNA. Finally, GRPR</span>⁺ neuron ablation eliminated scratching behavior in chronic itch mice regardless of whether the mice lacked CCR7.</div></div><div><h3>Conclusion</h3><div><span>Spinal CCR7 mediates persistent itch through a neural network with the inhibitory </span>neuropeptide NPY.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"119 2","pages":"Pages 64-72"},"PeriodicalIF":4.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144337384","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":"The joint meeting of the annual symposiums for KSSBR and PAPSBRS: Let's learn from its success for further development of skin barrier research","authors":"Yutaka Hatano ,&nbsp;Yoshikazu Uchida ,&nbsp;Takuya Takeichi","doi":"10.1016/j.jdermsci.2025.04.008","DOIUrl":"10.1016/j.jdermsci.2025.04.008","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"119 1","pages":"Pages 1-2"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144145253","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)00106-9","DOIUrl":"10.1016/S0923-1811(25)00106-9","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"119 1","pages":"Page ii"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144366392","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":"Big data-driven target identification by machine learning: DRD2 as a therapeutic target for psoriasis","authors":"Takashi Sakai ,&nbsp;Ryusuke Sawada ,&nbsp;Otoha Ichinose ,&nbsp;Takeshi Terabayashi ,&nbsp;Yutaka Hatano ,&nbsp;Yoshihiro Yamanishi ,&nbsp;Toshimasa Ishizaki","doi":"10.1016/j.jdermsci.2025.04.012","DOIUrl":"10.1016/j.jdermsci.2025.04.012","url":null,"abstract":"<div><h3>Background</h3><div>The development of medical treatments has traditionally relied on researchers leveraging scientific knowledge to hypothesize disease mechanisms and identify therapeutic agents. However, the depletion of novel therapeutic targets has become a significant challenge, resulting in stagnation within pharmaceutical research.</div></div><div><h3>Objective</h3><div>To address the scarcity of therapeutic targets, we developed a machine learning (ML)-based system capable of predicting therapeutic target molecules for diseases. To validate its utility, we applied this system to psoriasis, aiming to identify novel treatment strategies.</div></div><div><h3>Methods</h3><div>Our approach utilized a large clinical database to calculate reporting odds ratios for all drugs associated with the prevention of diseases of interest. We identified target proteins by analyzing large chemical structure databases to discover proteins commonly associated with preventive drug candidates. Experimental validation was conducted by administering a predicted therapeutic candidate in an imiquimod-induced psoriasis mouse model.</div></div><div><h3>Results</h3><div>The ML-based predictions identified drugs for Parkinson’s disease as potential preventive candidates for psoriasis. Further analysis highlighted dopamine receptor D2 (DRD2) as a therapeutic target. Administration of a DRD2 agonist alleviated psoriasis symptoms in mice, evidenced by the downregulation of mRNA expression in the IL-17 pathway and reduced serum tumor necrosis factor-α levels.</div></div><div><h3>Conclusion</h3><div>This study demonstrates the utility of a novel ML-based system for identifying therapeutic targets, as shown by its successful application in uncovering the role of DRD2 in psoriasis. Beyond psoriasis, this system offers significant potential for exploring pathological mechanisms and discovering therapeutic targets across various diseases.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"119 1","pages":"Pages 9-17"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144145252","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":"Algae ferment regulates initiation, amplification, and resolution of inflammation","authors":"Jaime Emmetsberger ,&nbsp;Donald Collins ,&nbsp;Nevena Karaman-Jurukovska ,&nbsp;Amanda Messina ,&nbsp;Dawn Layman ,&nbsp;Thomas Mammone ,&nbsp;Kenji Kabashima ,&nbsp;Nadine Pernodet","doi":"10.1016/j.jdermsci.2025.04.005","DOIUrl":"10.1016/j.jdermsci.2025.04.005","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"119 1","pages":"Pages 43-45"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144055573","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}