Journal of dermatological science最新文献

{"title":"EDA-A2 increases lipid production in EDA2R-expressing human sebocytes","authors":"Mi Hee Kwack, Ons Ben Hamida, Weon Ju Lee, Moon Kyu Kim","doi":"10.1016/j.jdermsci.2023.11.005","DOIUrl":"10.1016/j.jdermsci.2023.11.005","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"113 1","pages":"Pages 34-37"},"PeriodicalIF":4.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181123002438/pdfft?md5=06e4e544c502757e0a662ab483ac694a&pid=1-s2.0-S0923181123002438-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138465236","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":"Comparison of skin barrier abnormalities and epidermal ceramide profiles among three ω-O-acylceramide synthesis-deficient mouse strains","authors":"Yuta Yamamoto,&nbsp;Takayuki Sassa,&nbsp;Akio Kihara","doi":"10.1016/j.jdermsci.2023.12.003","DOIUrl":"10.1016/j.jdermsci.2023.12.003","url":null,"abstract":"<div><h3>Background</h3><p>The epidermis contains many structurally diverse ceramides, which form the skin permeability barrier (skin barrier). Mutations in genes involved in the synthesis of ω-<em>O</em>-acylceramides (acylceramides) and protein-bound ceramides cause ichthyosis.</p></div><div><h3>Objective</h3><p>We aimed to elucidate the relationship between the degree of skin barrier impairment and changes in epidermal ceramide profiles caused by mutations in acylceramide synthesis genes.</p></div><div><h3>Methods</h3><p>Knockout (KO) mice of three genes—fatty acid (FA) ω-hydroxylase <em>Cyp4f39</em> (human <em>CYP4F22</em> ortholog), FA elongase <em>Elovl1</em>, and acyl-CoA synthetase <em>Fatp4</em>—were subjected to transepidermal water loss measurement, toluidine blue staining, and epidermal ceramide profiling via liquid chromatography coupled with tandem mass spectrometry.</p></div><div><h3>Results</h3><p>Transepidermal water loss was highest in <em>Cyp4f39</em> KO mice, followed by <em>Elovl1</em> KO and <em>Fatp4</em> KO mice, and <em>Cyp4f39</em> KO mice also showed the strongest degree of toluidine blue staining. In <em>Cyp4f39</em> KO, <em>Elovl1</em> KO, and <em>Fatp4</em> KO mice, acylceramide levels were 0.6%, 1.6%, and 12%, respectively, of those in wild-type mice. Protein-bound ceramide levels were 0.2%, 30%, and 33%, respectively, of those in wild-type mice. We also observed a near-complete absence of ω-hydroxy ceramides in <em>Cyp4f39</em> KO mice, reduced total ceramide levels and shortened FA moieties in <em>Elovl1</em> KO mice, and increased hydroxylated ceramide levels and slightly shortened FA moieties in <em>Fatp4</em> KO mice.</p></div><div><h3>Conclusions</h3><p>The degree of reduction in protein-bound ceramide levels is probably related to the severity of skin barrier defects in these three strains. However, reduced acylceramide levels and other changes in ceramide composition unique to each KO strain are also involved.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"113 1","pages":"Pages 10-17"},"PeriodicalIF":4.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181123002530/pdfft?md5=68738f63a9acc9d97398d25527c80898&pid=1-s2.0-S0923181123002530-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138569312","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":"Low-dose imiquimod induces melanogenesis in melanoma cells through an ROS-mediated pathway","authors":"Zheng-Yi Li ,&nbsp;Shu-Hao Chang ,&nbsp;Kuang-Ting Liu ,&nbsp;Alaina Edelie Wu ,&nbsp;Chien-Sheng Hsu ,&nbsp;Shi-Wei Huang ,&nbsp;Mu-Chi Chung ,&nbsp;Shih-Chung Wang ,&nbsp;Jun-Kai Kao ,&nbsp;Yi-Ju Chen ,&nbsp;Jeng-Jer Shieh","doi":"10.1016/j.jdermsci.2023.12.005","DOIUrl":"10.1016/j.jdermsci.2023.12.005","url":null,"abstract":"<div><h3>Background</h3><p>Melanogenesis is the process of melanin maturation which not only protects skin from UV radiation but also plays an important role in antigenicity of melanomas. Imiquimod (IMQ) is a toll-like receptor 7 (TLR7) agonist that exhibits antiviral and anticancer activity.</p></div><div><h3>Objective</h3><p>To explore whether IMQ could induce melanogenesis in melanoma cells.</p></div><div><h3>Methods</h3><p>The mouse melanoma cell line B16F10, the mouse immortalized melanocyte Melan-A, and human melanoma cell lines MNT-1, C32 and A375 were utilized in this study. The pigmented level was observed by the centrifuged cell pellet. The intracellular and extracellular melanin levels were examined in the absorbance in NaOH-extracted cell lysate and cell-cultured medium, respectively. The expression of melanogenesis related proteins was examined by immunoblotting. The intracellular cyclic AMP amount was evaluated by the cAMP Glo assay kit. The activity of phosphodiesterase 4B (PDE4B) was investigated by CREB reporter assay with overexpressed PDE4B or not.</p></div><div><h3>Results</h3><p>We demonstrated that a low dose of IMQ could trigger melanogenesis in B16F10 cells. IMQ induced microphthalmia-associated transcription factor (MITF) nuclear translocation, upregulated the expression of melanogenesis-related proteins, increased tyrosinase (TYR) activity, and led to pigmentation in B16F10 cells. Next, we found that IMQ-induced melanogenesis was activated by excessive intracellular cAMP accumulation, which was regulated through IMQ-mediated PDE4B inhibition. Finally, IMQ-induced ROS production was found to be involved in melanogenesis by its control of PDE4B activity.</p></div><div><h3>Conclusions</h3><p>Low dose of IMQ could activate melanogenesis through the ROS/PDE4B/PKA pathway in melanoma cells.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"113 1","pages":"Pages 18-25"},"PeriodicalIF":4.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181123002682/pdfft?md5=e1076029cba3585ea1eb90f735db9d14&pid=1-s2.0-S0923181123002682-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139020882","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":"A modified Sobel filter-based automated numerical algorithm enables immediate trichoscopic assessment of hair diameter diversity in male and female pattern hair loss","authors":"Masaya Takagi,&nbsp;Misaki Kinoshita-Ise,&nbsp;Masahiro Fukuyama,&nbsp;Soichiro Aoki,&nbsp;Saori Nishikawa,&nbsp;Mami Miyoshi,&nbsp;Takaki Sugimoto,&nbsp;Masako Yamazaki,&nbsp;Masashi Ogo,&nbsp;Manabu Ohyama","doi":"10.1016/j.jdermsci.2023.11.004","DOIUrl":"10.1016/j.jdermsci.2023.11.004","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"113 1","pages":"Pages 38-40"},"PeriodicalIF":4.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181123002426/pdfft?md5=73bacd952979a502d093f9340a76e1d5&pid=1-s2.0-S0923181123002426-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138465235","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(24)00006-9","DOIUrl":"https://doi.org/10.1016/S0923-1811(24)00006-9","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"113 1","pages":"Page 1"},"PeriodicalIF":4.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181124000069/pdfft?md5=9444821a685fc43e69e8c6bf6b2d0013&pid=1-s2.0-S0923181124000069-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139699338","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":"High migratory activity of dermal sheath cup cells associated with the clinical efficacy of autologous cell-based therapy for pattern hair loss","authors":"Yumiko Ishimatsu-Tsuji ,&nbsp;Shiro Niiyama ,&nbsp;Ryokichi Irisawa ,&nbsp;Kazutoshi Harada ,&nbsp;Jiro Kishimoto ,&nbsp;Ryoji Tsuboi","doi":"10.1016/j.jdermsci.2023.11.003","DOIUrl":"10.1016/j.jdermsci.2023.11.003","url":null,"abstract":"<div><h3>Background</h3><p>Autologous cell-based therapy using dermal sheath cup (DSC) cells was reported as a new treatment for male and female pattern hair loss. However, the mechanisms underlying its action remain unclear.</p></div><div><h3>Objective</h3><p>We investigated the mechanisms underlying the efficacy of DSC cells in cell-based therapy.</p></div><div><h3>Methods</h3><p>We conducted multivariate analysis to categorize individuals based on treatment response as responders and non-responders. The differentially expressed genes in DSC cells from the two groups were evaluated using bulk transcriptome, quantitative polymerase chain reaction, and single-cell transcriptome analyses. We performed live cell imaging combined with immunostaining to characterize the DSC subpopulation associated with responders.</p></div><div><h3>Results</h3><p>We identified nine and three genes as high efficacy (HE) and low efficacy (LE) marker genes, respectively. The HE subpopulations were enriched for cell migration-related genes in single-cell analysis. In contrast, the LE subpopulation was enriched for basement membrane and vasculature-related genes. Moreover, DSC cells in culture were immunocytochemically and morphologically heterogeneous, expressing characteristic factors. Furthermore, live cell imaging showed that DSC cells expressing integrin subunit alpha 6 (ITGA6), an HE subpopulation gene, had markedly higher mobility than those expressing the LE subpopulation genes collagen type IV or CD36.</p></div><div><h3>Conclusions</h3><p>ITGA6-positive DSC cells, with superior migratory activity, may contribute to cell-based therapy by promoting cell migration into nearby hair follicles.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"113 1","pages":"Pages 26-33"},"PeriodicalIF":4.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181123002414/pdfft?md5=edfa610e798cd3f1b2fb6eed9771d813&pid=1-s2.0-S0923181123002414-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135615370","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":"High glucose environment induces NEDD4 deficiency that impairs angiogenesis and diabetic wound healing","authors":"Yu Guo,&nbsp;Yongjie Wang,&nbsp;Haiwei Liu,&nbsp;Xulei Jiang,&nbsp;Shaorong Lei","doi":"10.1016/j.jdermsci.2023.09.007","DOIUrl":"10.1016/j.jdermsci.2023.09.007","url":null,"abstract":"<div><h3>Background</h3><p>Healing of diabetic wounds, characterized by impaired angiogenesis<span>, remains a clinical challenge. E3 ligase have been identified as potential therapeutic targets of wound healing.</span></p></div><div><h3>Objective</h3><p>We assessed the role of E3 ligase NEDD4 in the context of angiogenesis and diabetic wound healing.</p></div><div><h3>Methods</h3><p><span>The mRNA expression levels of NEDD4, TSP1<span><span> and VEGF were determined by real-time PCR. Western blotting was used to evaluate the </span>protein expression of NEDD4, TSP1 and VEGF. The </span></span>ubiquitination<span><span> of TSP1 was evaluated by immunoprecipitation. </span>MTT assay<span><span>, wound healing assay and tube formation assay were performed to assess the proliferation, migration and angiogenic functions of endothelial cells. The </span>epigenetic modification in the promoter of NEDD4 was confirmed using BSP assay and ChIP-qPCR assay. The role of NEDD4 in wound healing was further verified in diabetic mouse model.</span></span></p></div><div><h3>Results</h3><p>NEDD4 promotes proliferation, migration and tube formation of endothelial cells. It binds to and ubiquitinates TSP1, which lead to TSP1 degradation and thus increased VEGF expression. The inhibitory effect of NEDD4 silencing on the angiogenesis ability of endothelial cells can be restored by TSP1 knockdown. NEDD4 is reduced in diabetic patients, which may due to hypermethylation of NEDD4 promoter mediated via DNMT1 under high glucose condition. Furthermore, inhibition of NEDD4 represses wound healing in diabetic mouse model.</p></div><div><h3>Conclusion</h3><p>NEDD4 might promote angiogenesis and wound healing by inhibiting TSP1 via ubiquitination in diabetic patients.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"112 3","pages":"Pages 148-157"},"PeriodicalIF":4.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71490526","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":"Alopecia areata: What’s new in the epidemiology, comorbidities, and pathogenesis?","authors":"Teruki Dainichi ,&nbsp;Masashi Iwata ,&nbsp;Yo Kaku","doi":"10.1016/j.jdermsci.2023.09.008","DOIUrl":"10.1016/j.jdermsci.2023.09.008","url":null,"abstract":"<div><h3>Background</h3><p><span>Alopecia areata<span> (AA) is a common, acquired, and nonscarring type of hair loss that affects people of every generation and is intractable in severe and relapsing cases. Patients with AA, especially those with greater scalp involvement, have poor health-related quality-of-life scores. Purpose: Following our previous review article in the April 2017 issue of the Journal of Dermatological Science, we aim to provide a pair of review articles on recent progress in multidisciplinary approaches to AA. Main findings: We found more than 1800 publications on AA from July 2016 to December 2022. Conclusions: In this review, we focused on the latest information on the </span></span>epidemiology, comorbidities, and pathogenesis of AA.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"112 3","pages":"Pages 120-127"},"PeriodicalIF":4.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41224132","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":"METTL14-mediated N6-methyladenosine modification of Col17a1/Itgα6/Itgβ4 governs epidermal homeostasis","authors":"Renpeng Zhou ,&nbsp;Qirui Wang ,&nbsp;Siyi Zeng,&nbsp;Yimin Liang,&nbsp;Danru Wang","doi":"10.1016/j.jdermsci.2023.10.005","DOIUrl":"10.1016/j.jdermsci.2023.10.005","url":null,"abstract":"<div><h3>Background</h3><p>N6-methyladenosine (m⁶A) is the most abundant and reversible modification occurring in eukaryotic mRNAs, however, its functions in mammalian epidermal development are still not fully elucidated.</p></div><div><h3>Objective</h3><p>To explore the role of METTL14 (Methyltransferase like 14), one of the m⁶<span>A methyltransferases, in maintaining epidermal homeostasis.</span></p></div><div><h3>Methods</h3><p>We constructed mice with <em>Mettl14</em><span><span>-inactivation in the epidermal basal cells. The phenotype was explored by H&amp;E staining and </span>immunofluorescence staining. To explore the underlying mechanisms, we performed RNA-seq, Ribosome profiling and MeRIP-seq on wild-type and </span><em>Mettl14</em><span><span>-inactivation epidermal keratinocytes. Moreover, </span>HaCaT cells were used for </span><em>in vitro</em> validation.</p></div><div><h3>Results</h3><p>Inactivation of <em>Mettl14</em><span><span><span> in murine epidermis led to transient thicker epidermis and exhaustion of the epidermal stem cell pool. Interestingly, we found that the mRNA of </span>type XVII collagen (Col17a1), </span>integrin β4 (Itgβ4) and α6 (Itgα6) had m</span>⁶<span>A modifications, and the proteins expression were decreased in </span><em>Mettl14</em>-inactivated epidermis. Furthermore, in epidermis-specific <em>Mettl4</em><span><span>-inactivated mice, the epidermis was detached from the dermis and presented a phenotype similar to </span>junctional epidermolysis bullosa<span> (JEB), which may result from hemidesmosomes damage (decrease of COL17A1, ITGB4 and ITGA6). Knockdown of </span></span><em>Mettl14</em> in HaCaT cells impaired the self-renewal and decreased the protein level of COL17A1, ITGB4 and ITGA6 and <em>Itgβ4</em> knockdown inhibited colony formation.</p></div><div><h3>Conclusion</h3><p>Our study highlighted the role of METTL14 in the maintenance of epidermal homeostasis and identified its critical role through m⁶<span>A-mediated translational inhibition of Col17a1, Itgβ4 and Itgα6. Our study suggested that METTL14 may be a potential therapeutic target for the treatment of hemidesmosomes-deficient diseases, such as JEB.</span></p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"112 3","pages":"Pages 138-147"},"PeriodicalIF":4.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89721336","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":"Bath-psoralen plus UVA therapy changes inflammatory proteomic signatures for systemic effects beyond the skin","authors":"Yoshifumi Kanayama,&nbsp;Kyoko Ikumi,&nbsp;Mai Sakurai,&nbsp;Yuki Enomoto,&nbsp;Emi Nishida,&nbsp;Aya Yamamoto,&nbsp;Akimichi Morita","doi":"10.1016/j.jdermsci.2023.09.004","DOIUrl":"10.1016/j.jdermsci.2023.09.004","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"112 3","pages":"Pages 162-165"},"PeriodicalIF":4.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181123002165/pdfft?md5=46f250687336d77dd98930e4221b37b0&pid=1-s2.0-S0923181123002165-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71430543","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}