Journal of dermatological science最新文献

{"title":"20240927Announcement_JDSBestPaperAward","authors":"","doi":"10.1016/S0923-1811(24)00204-4","DOIUrl":"10.1016/S0923-1811(24)00204-4","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"116 1","pages":"Page 59"},"PeriodicalIF":4.6,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142533810","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":"Corrigendum to “Decreased TET2/5-hmC reduces the integrity of the epidermal barrier via epigenetic dysregulation of filaggrin in psoriatic lesions” [J. Dermatol. Sci. 113 (2024) 103–112]","authors":"Huan Zhang , Tao Jia , Delu Che , Bin Peng , Zhaowei Chu , Xiangjin Song , Weihui Zeng , Songmei Geng","doi":"10.1016/j.jdermsci.2024.07.003","DOIUrl":"10.1016/j.jdermsci.2024.07.003","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"115 3","pages":"Pages 147-148"},"PeriodicalIF":4.6,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S092318112400149X/pdfft?md5=4e402410281c340edd24c5104f5dfc9a&pid=1-s2.0-S092318112400149X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141880025","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":"Revealing the UV response of melanocytes in xeroderma pigmentosum group A using patient-derived induced pluripotent stem cells","authors":"Chihiro Takemori ,&nbsp;Michiyo Koyanagi-Aoi ,&nbsp;Takeshi Fukumoto ,&nbsp;Makoto Kunisada ,&nbsp;Kazumasa Wakamatsu ,&nbsp;Shosuke Ito ,&nbsp;Chieko Hosaka ,&nbsp;Seiji Takeuchi ,&nbsp;Akiharu Kubo ,&nbsp;Takashi Aoi ,&nbsp;Chikako Nishigori","doi":"10.1016/j.jdermsci.2024.06.004","DOIUrl":"10.1016/j.jdermsci.2024.06.004","url":null,"abstract":"<div><h3>Background</h3><p><span><span>Xeroderma pigmentosum (XP) is characterized by </span>photosensitivity<span><span> that causes pigmentary disorder and predisposition to skin cancers on sunlight-exposed areas due to </span>DNA repair deficiency. Patients with XP group A (XP-A) develop freckle-like pigmented maculae and depigmented maculae within a year unless strict sun-protection is enforced. Although it is crucial to study </span></span>pigment cells (melanocytes: MCs) as disease target cells, establishing MCs in primary cultures is challenging.</p></div><div><h3>Objective</h3><p><span>Elucidation of the disease pathogenesis by comparison between MCs differentiated from XP-A induced pluripotent stem cells (iPSCs) and healthy control iPSCs on the response to </span>UV irradiation.</p></div><div><h3>Methods</h3><p><span>iPSCs were established from a XP-A fibroblasts and differentiated into MCs. Differences in gene expression profiles between XP-A-iPSC-derived melanocytes (XP-A-iMCs) and Healthy control iPSC-derived MCs (HC-iMCs) were analyzed 4 and 12 h after irradiation with 30 or 150 J/m</span>²<span> of UV-B using microarray analysis.</span></p></div><div><h3>Results</h3><p><span><span>XP-A-iMCs expressed SOX10, </span>MITF<span>, and TYR, and showed melanin synthesis<span><span>. Further, XP-A-iMCs showed reduced DNA repair ability. Gene expression profile between XP-A-iMCs and HC-iMCs revealed that, numerous </span>gene probes that were specifically upregulated or downregulated in XP-A-iMCs after 150-J/m</span></span></span>² of UV-B irradiation did not return to basal levels. Of note that apoptotic pathways were highly upregulated at 150 J/m² UV exposure in XP-A-iMCs, and cytokine-related pathways were upregulated even at 30 J/m² UV exposure.</p></div><div><h3>Conclusion</h3><p>We revealed for the first time that cytokine-related pathways were upregulated even at low-dose UV exposure in XP-A-iMCs. Disease-specific iPSCs are useful to elucidate the disease pathogenesis and develop treatment strategies of XP.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"115 3","pages":"Pages 111-120"},"PeriodicalIF":4.6,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141736215","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":"Cold shock therapy promotes hair growth in association with upregulation of cold-inducible RNA-binding protein and vascular endothelial growth factor","authors":"Seunghee Lee ,&nbsp;Sanseul Kim ,&nbsp;Sungjoo Tommy Hwang ,&nbsp;Gun-Ho Kim ,&nbsp;Ohsang Kwon","doi":"10.1016/j.jdermsci.2024.08.001","DOIUrl":"10.1016/j.jdermsci.2024.08.001","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"115 3","pages":"Pages 141-144"},"PeriodicalIF":4.6,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142057676","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":"Corrigendum to “Dual effect of tacrolimus on mast cell-mediated allergy and inflammation through MAS-related G protein-coupled receptor-X2” [J. Dermatol. Sci. 112 (2023) 128–137]","authors":"Xueshan Du ,&nbsp;Delu Che ,&nbsp;Bin Peng ,&nbsp;Yi Zheng ,&nbsp;Yong Hao ,&nbsp;Tao Jia ,&nbsp;Xinyue Zhang ,&nbsp;Songmei Geng","doi":"10.1016/j.jdermsci.2024.06.005","DOIUrl":"10.1016/j.jdermsci.2024.06.005","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"115 3","pages":"Pages 145-146"},"PeriodicalIF":4.6,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181124001385/pdfft?md5=380049bd5002a76a77f44bf2926f67ec&pid=1-s2.0-S0923181124001385-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141861984","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":"Semaxanib, a VEGF inhibitor, suppresses melanogenesis by modulating CRTC3 independently of VEGF signaling","authors":"HyeJi Kwon ,&nbsp;Jeong Hyeon Lee ,&nbsp;Jae Min Yoo ,&nbsp;Huonggiang Nguyen ,&nbsp;Hongchan An ,&nbsp;Sung Eun Chang ,&nbsp;Youngsup Song","doi":"10.1016/j.jdermsci.2024.07.004","DOIUrl":"10.1016/j.jdermsci.2024.07.004","url":null,"abstract":"<div><h3>Background</h3><p>Dysregulation of melanogenesis contributes to the development of skin hyperpigmentation diseases, which poses a treatment challenge. Following the establishment of CRTC3 screening methods to explore small molecules inhibiting melanogenesis for the topical treatment of hyperpigmentation diseases, we identified a candidate molecule, semaxanib.</p></div><div><h3>Objective</h3><p>To explore the antimelanogenic effects of semaxanib, a vascular endothelial growth factor receptor (VEGFR) 2 inhibitor, for potential applications in hyperpigmentation management and to unravel the role of VEGF signaling in melanocyte biology by investigating mechanism of action of semaxanib.</p></div><div><h3>Methods</h3><p>Mouse-derived spontaneously immortalized melanocytes, B16F10, and normal human primary epidermal melanocytes cells were treated with semaxanib, and cellular responses were assessed using cell viability assays and melanin content measurements. Molecular mechanisms were investigated using transcriptional activity assays, reverse-transcription polymerase chain reaction, and immunoblotting analysis. <em>In vivo</em> studies were conducted using an epidermis-humanized transgenic mouse model and <em>ex vivo</em> human skin tissues.</p></div><div><h3>Results</h3><p>Semaxanib ameliorated melanin content in cultured melanocytes by downregulating the expression of melanogenesis-associated genes by suppressing the CRTC3/microphthalmia-associated transcription factors. Topical application of semaxanib reduced melanin accumulation in the ultraviolet B–stimulated <em>ex vivo</em> human epidermis and tail of K14-stem cell factor transgenic mice. Mechanistically, the antimelanogenic effect induced by semaxanib was associated with SIK2-CRTC3-MITF rather than VEGF signaling in melanocytes.</p></div><div><h3>Conclusion</h3><p>Semaxanib emerges as a promising candidate for the development of therapeutics for hyperpigmentation, potentially working independently of VEGF signaling in human melanocytes.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"115 3","pages":"Pages 121-129"},"PeriodicalIF":4.6,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141845138","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":"JSID flier with late breaking announce","authors":"","doi":"10.1016/S0923-1811(24)00186-5","DOIUrl":"10.1016/S0923-1811(24)00186-5","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"115 3","pages":"Page I"},"PeriodicalIF":4.6,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142244197","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":"Exposure to volatile ferroptosis inhibitor, TEMPO, reduced cutaneous ischemia-reperfusion injury progression to pressure ulcer formation in a mouse model","authors":"Mai Ishikawa ,&nbsp;Akihiko Uchiyama ,&nbsp;Keiji Kosaka ,&nbsp;Mayu Nishio ,&nbsp;Sachiko Ogino ,&nbsp;Yoko Yokoyama ,&nbsp;Ryoko Torii ,&nbsp;Ryoko Akai ,&nbsp;Takao Iwawaki ,&nbsp;Seiji Torii ,&nbsp;Sei-ichiro Motegi","doi":"10.1016/j.jdermsci.2024.07.005","DOIUrl":"10.1016/j.jdermsci.2024.07.005","url":null,"abstract":"<div><h3>Background</h3><p>Ischemia– reperfusion (I/R) injury-induced oxidative stress is a key factor in the pathogenesis of pressure ulcer formation. Ferroptosis is an iron-dependent programmed cell death that connects oxidative stress and inflammation in various diseases. Recent studies revealed the protective effect of inhibition of ferroptosis in I/R injury. However, the role of ferroptosis in cutaneous I/R injury remains elusive.</p></div><div><h3>Objective</h3><p>To assess the role of ferroptosis in the progression of cutaneous I/R injury.</p></div><div><h3>Methods</h3><p>Cutaneous I/R injury experiments and histopathological studies were performed in wild-type mice with or without exposure to volatile ferroptosis inhibitor, TEMPO (2,2,6,6-Tetramethylpiperidine-1-oxyl). The suppressive effects of TEMPO on ferroptosis inducing cell death and oxidative stress were examined <em>in vitro</em>.</p></div><div><h3>Results</h3><p>Inhibition of ferroptosis with TEMPO significantly reduced ulcer formation after cutaneous I/R injury. Fluctuated ferroptosis markers, such as GPX4, ACSL4, and 4-HNE expression in the I/R skin site, were reversed by TEMPO treatment. Inhibition of ferroptosis reduced apoptosis, CD3⁺ infiltrating lymphocytes, and improved vascularity in the I/R skin site. Inhibition of ferroptosis also suppressed the enhancement of Nrf2 activation. <em>In vitro</em>, ferroptosis and the activation of ferroptosis-related gene expression by RSL3 stimulation were markedly ameliorated by TEMPO treatment in mouse fibroblasts. Inhibiting ferroptosis also suppressed the elevation of the mRNA levels of NOX2 and HO-1 caused by ferroptosis.</p></div><div><h3>Conclusion</h3><p>Cutaneous I/R injury-induced ferroptosis likely promotes cell death, vascular loss, infiltration of inflammatory cells, and oxidative stress. The inhibition of ferroptosis with TEMPO might have potential clinical application as novel therapeutic agent for cutaneous I/R injury.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"115 3","pages":"Pages 130-140"},"PeriodicalIF":4.6,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181124001518/pdfft?md5=ada58dbe07a87acdcb729adcccd7d6b0&pid=1-s2.0-S0923181124001518-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141853815","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":"Optimization of an adeno-associated viral vector for epidermal keratinocytes in vitro and in vivo","authors":"Qi Shen ,&nbsp;Shogo Suga ,&nbsp;Yuta Moriwaki ,&nbsp;Zening Du ,&nbsp;Emi Aizawa ,&nbsp;Mutsumi Okazaki ,&nbsp;Juan Carlos Izpisua Belmonte ,&nbsp;Yusuke Hirabayashi ,&nbsp;Keiichiro Suzuki ,&nbsp;Masakazu Kurita","doi":"10.1016/j.jdermsci.2024.07.006","DOIUrl":"10.1016/j.jdermsci.2024.07.006","url":null,"abstract":"<div><h3>Background</h3><p>Local gene therapies, including <em>in vivo</em> genome editing, are highly anticipated for the treatment of genetic diseases in skin, especially the epidermis. While the adeno-associated virus (AAV) is a potent vector for <em>in vivo</em> gene delivery, the lack of efficient gene delivery methods has limited its clinical applications.</p></div><div><h3>Objective</h3><p>To optimize the AAV gene delivery system with higher gene delivery efficiency and specificity for epidermis and keratinocytes (KCs), using AAV capsid and promoter engineering technologies.</p></div><div><h3>Methods</h3><p>AAV variants with mutations in residues reported to be critical to determine the tropism of AAV2 for KCs were generated by site-directed mutagenesis of AAVDJ. The infection efficiency and specificity for KCs of these variants were compared with those of previously reported AAVs considered to be suitable for gene delivery to KCs <em>in vitro</em> and <em>in vivo</em>. Additionally, we generated an epidermis-specific promoter using the most recent short-core promoter and compared its specificity with existing promoters.</p></div><div><h3>Results</h3><p>A novel AAVDJ variant capsid termed AAVDJK2 was superior to the existing AAVs in terms of gene transduction efficiency and specificity for epidermis and KCs <em>in vitro</em> and <em>in vivo</em>. A novel tissue-specific promoter, termed the K14 SCP3 promoter, was superior to the existing promoters in terms of gene transduction efficiency and specificity for KCs.</p></div><div><h3>Conclusion</h3><p>The combination of the AAVDJK2 capsid and K14 SCP3 promoter improves gene delivery to epidermis <em>in vivo</em> and KCs <em>in vitro</em>. The novel AAV system may benefit experimental research and development of new epidermis-targeted gene therapies.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"115 3","pages":"Pages 101-110"},"PeriodicalIF":4.6,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141914943","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":"Enhancement of skin barrier function and augmentation of epidermal cell-cell interactions by galactomyces ferment filtrate","authors":"Satoshi Nakamizo ,&nbsp;Xianghong Yan ,&nbsp;Kenji Kabashima","doi":"10.1016/j.jdermsci.2024.03.011","DOIUrl":"10.1016/j.jdermsci.2024.03.011","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"115 2","pages":"Pages 94-97"},"PeriodicalIF":4.6,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181124000574/pdfft?md5=8d0fd39403ab5f87104e964e890f7e1d&pid=1-s2.0-S0923181124000574-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141629557","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}