Journal of dermatological science最新文献

{"title":"Editor's Choice","authors":"","doi":"10.1016/S0923-1811(24)00075-6","DOIUrl":"https://doi.org/10.1016/S0923-1811(24)00075-6","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"114 2","pages":"Page 53"},"PeriodicalIF":4.6,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181124000756/pdfft?md5=adbba30d23dce64344f0b5ac840c8365&pid=1-s2.0-S0923181124000756-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141090275","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":"DNA repair ability in a patient with voriconazole-related squamous cell carcinoma that required differential diagnosis from xeroderma pigmentosum","authors":"Takeshi Fukumoto , Tomoka Harada , Takamichi Ito , Satoshi Fukushima , Ryusuke Ono , Masutaka Furue , Chikako Nishigori","doi":"10.1016/j.jdermsci.2024.02.005","DOIUrl":"10.1016/j.jdermsci.2024.02.005","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"114 2","pages":"Pages 83-85"},"PeriodicalIF":4.6,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140804429","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":"Proteome characterization of XPC-deficient melanocytes generated by CRISPR-Cas9 technology reveals alteration in the expression of several hundred proteins","authors":"Muriel Cario , Julie Scalia , Walid Mahfouf , Elodie Muzotte , Vincent Michaud , Claudio Plaisant , Jean-William Dupuy , Thierry Douki , Fanny Morice-Picard , Jérôme Rambert , Eric Perrier , Sandra Trompezinski , Hamid-Reza Rezvani","doi":"10.1016/j.jdermsci.2024.03.006","DOIUrl":"10.1016/j.jdermsci.2024.03.006","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"114 2","pages":"Pages 79-82"},"PeriodicalIF":4.6,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140277131","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":"Visualization of intradermal blood vessel structures by dual-wavelength photoacoustic microscopy and characterization of three-dimensional construction of livedo-racemosa in cutaneous polyarteritis nodosa","authors":"Kazuyo Sujino ,&nbsp;Keiji Tanese ,&nbsp;Yasuko Saito ,&nbsp;Junko Kuramoto ,&nbsp;Hideaki Iwazaki ,&nbsp;Taiichiro Ida ,&nbsp;Sadakazu Aiso ,&nbsp;Nobuaki Imanishi ,&nbsp;Hiroki Kajita ,&nbsp;Keitaro Fukuda ,&nbsp;Masayuki Amagai ,&nbsp;Akiko Tanikawa","doi":"10.1016/j.jdermsci.2024.03.010","DOIUrl":"10.1016/j.jdermsci.2024.03.010","url":null,"abstract":"<div><h3>Background</h3><p>Photoacoustic microscopy is expected to have clinical applications as a noninvasive and three-dimensional (3D) method of observing intradermal structures.</p></div><div><h3>Objective</h3><p>Investigate the applicability of a photoacoustic microscope equipped with two types of pulsed lasers that can simultaneously recognize hemoglobin and melanin.</p></div><div><h3>Methods</h3><p>16 skin lesions including erythema, pigmented lesions, vitiligo and purpura, were analyzed to visualize 3D structure of melanin granule distribution and dermal blood vessels. 13 cases of livedo racemosa in cutaneous polyarteritis nodosa (cPN) were further analyzed to visualize the 3D structure of dermal blood vessels in detail. Vascular structure was also analyzed in the biopsy specimens obtained from tender indurated erythema of cPN by CD34 immunostaining.</p></div><div><h3>Results</h3><p>Hemoglobin-recognition signal clearly visualized the 3D structure of dermal blood vessels and melanin-recognition signal was consistently reduced in vitiligo. In livedo racemosa, the hemoglobin-recognition signal revealed a relatively thick and large reticular structure in the deeper layers that became denser and finer toward the upper layers. The numerical analysis revealed that the number of dermal blood vessels was 1.29-fold higher (p&lt;0.05) in the deeper region of the lesion than that of normal skin. The CD34 immunohistochemical analysis in tender indurated erythema revealed an increased number of dermal vessels compared with normal skin in 88.9% (8/9) of the cases, suggesting that vascular network remodeling had occurred in cPN.</p></div><div><h3>Conclusion</h3><p>The photoacoustic system has an advantage in noninvasively detecting dermal blood vessel structures that are difficult to recognize by two-dimensional histopathology specimen examination and is worth evaluating in various skin diseases.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"114 2","pages":"Pages 71-78"},"PeriodicalIF":4.6,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181124000562/pdfft?md5=7d7bfd13601c7ef9c5cc256f9d4d7104&pid=1-s2.0-S0923181124000562-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140405902","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":"Lack of cutis verticis gyrata is associated with c.1279_1290del12 of SLCO2A1 in 43 Japanese patients with pachydermoperiostosis","authors":"H. Niizeki ,&nbsp;R. Tanaka ,&nbsp;T. Nomura ,&nbsp;A. Seki ,&nbsp;M. Miyasaka ,&nbsp;Y. Matsumoto ,&nbsp;M. Ishibashi ,&nbsp;S. Narumi ,&nbsp;K. Nakabayashi ,&nbsp;K. Yoshida","doi":"10.1016/j.jdermsci.2024.03.008","DOIUrl":"10.1016/j.jdermsci.2024.03.008","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"114 2","pages":"Pages 86-88"},"PeriodicalIF":4.6,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140399792","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":"IL-4-induced decrease in both the number and CTLA-4 expression of Treg impairs suppression of Th2 type inflammation in severe atopic dermatitis","authors":"Bocheng Wang ,&nbsp;Zhiying Yu ,&nbsp;Jiao Liu ,&nbsp;Yuyang Tian ,&nbsp;Yijia Ruan ,&nbsp;Tinghui Kong ,&nbsp;Mingjun Hou ,&nbsp;Bihui Yu ,&nbsp;Shiqi Ling ,&nbsp;Di Wang ,&nbsp;Yishan Chen ,&nbsp;Yingping Xu ,&nbsp;Weiwei Deng ,&nbsp;Yunsheng Liang","doi":"10.1016/j.jdermsci.2024.03.007","DOIUrl":"10.1016/j.jdermsci.2024.03.007","url":null,"abstract":"<div><h3>Background</h3><p>T_reg plays a pivotal role in the suppression of Th2 cell and the maintenance of immune homeostasis. The precise molecular mechanism underlying the disruption of T_reg suppression of Th2 cell and the promotion of Th2 type inflammation in allergic diseases remains elusive.</p></div><div><h3>Objective</h3><p>This study aims to investigate the molecular mechanism underlying quantitative and functional changes of T_reg in AD.</p></div><div><h3>Methods</h3><p>The molecular mechanism was investigated using flow cytometry, mRNA sequencing, co-culture experiments, co-immunoprecipitation, chromatin immunoprecipitation, and bisulfite sequencing in vitro or in AD mice model and patients with AD.</p></div><div><h3>Results</h3><p>Increased proportion of T_reg was detected in mild and moderate AD. Conversely, characteristic decrease in both the number and CTLA-4 expression of T_reg was relevant to serum IL-4 level in severe AD patients, which was verified under a high concentration of IL-4 treatment in vitro. The underlying mechanism is that IL-4/pSTAT6 pathway recruits DNMT1 and HDAC2 to inhibit transcriptional regulation of Foxp3 and CTLA-4 loci. High level of IL-4 impaired the suppression of T_reg against Th2 cell differentiation mediated by CTLA-4, and blockade of IL-4Rα signaling in T_reg restored T_reg number and suppression of Th2 cell in AD model mice and patients with AD.</p></div><div><h3>Conclusion</h3><p>The number of T_reg is relevant to stratification of severity and serum IL-4 level in patients with AD. Abnormal high level of IL-4 epigenetically triggers a decrease in both the number and CTLA-4 expression of T_reg. The reduced expression of CTLA-4 on T_reg induced by IL-4 impairs suppression of Th2 cell differentiation.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"114 2","pages":"Pages 54-63"},"PeriodicalIF":4.6,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140276538","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":"KTN1 mediated unfolded protein response protects keratinocytes from ionizing radiation-induced DNA damage","authors":"Xinli Niu ,&nbsp;Yi Shen ,&nbsp;Yunhan Wen,&nbsp;Xing Mi,&nbsp;Jing Xie,&nbsp;Ying Zhang,&nbsp;Zhenhua Ding","doi":"10.1016/j.jdermsci.2024.02.006","DOIUrl":"10.1016/j.jdermsci.2024.02.006","url":null,"abstract":"<div><h3>Background</h3><p>The unfolded protein response (UPR) is one of the cytoprotective mechanisms against various stresses and essential for the normal function of skin. Skin injury caused by ionizing radiation (IR) is a common side effect of radiotherapy and it is unclear how UPR affects IR-induced skin injury.</p></div><div><h3>Objectives</h3><p>To verify the effect of UPR on IR-induced DNA damage in keratinocytes and the relation between an endoplasmic reticulum (ER) protein KTN1 and UPR.</p></div><div><h3>Methods</h3><p>All experiments were performed on keratinocytes models: HaCaT and HEK-A. ER lumen and the expression levels of KTN1 and UPR pathway proteins (PERK, IRE1α and ATF6) were examined by transmission electron microscopy and immunoblotting, respectively. 4-PBA, an UPR inhibitor, was used to detected its effects on DNA damage and cell proliferation. Subsequently, the effects of KTN1 deletion on UPR, DNA damage and cell proliferation after IR were detected. Tunicamycin was used to reactivate UPR and then we examined its effects on DNA damage.</p></div><div><h3>Results</h3><p>UPR was activated by IR in keratinocytes. Inhibition of UPR aggravated DNA damage and suppressed cell proliferation after IR. KTN1 expression was upregulated by IR and KTN1 depletion reduced ER expansion and the expression of UPR-related proteins. Moreover, KTN1 depletion aggravated DNA damage and suppressed cell proliferation after IR could reversed by reactivation of UPR.</p></div><div><h3>Conclusion</h3><p>KTN1 deletion aggravates IR-induced keratinocyte DNA damage via inhibiting UPR. Our findings provide new insights into the mechanisms of keratinocytes in response to IR-induced damage.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"114 1","pages":"Pages 24-33"},"PeriodicalIF":4.6,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S092318112400029X/pdfft?md5=739856660a84c089c0e3b2d867ba71a2&pid=1-s2.0-S092318112400029X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140011371","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":"JSID’s Fellowship Shiseido Research Grant","authors":"Manabu Ohyama (Secretary-General of JSID)","doi":"10.1016/j.jdermsci.2024.03.005","DOIUrl":"10.1016/j.jdermsci.2024.03.005","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"114 1","pages":"Page 52"},"PeriodicalIF":4.6,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181124000513/pdfft?md5=f8c7392085493305488051f6e1f0026f&pid=1-s2.0-S0923181124000513-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140156442","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":"Rh family C glycoprotein contributes to psoriatic inflammation through regulating the dysdifferentiation and cytokine secretion of keratinocytes","authors":"Wei Liu,&nbsp;Yaqi Wang,&nbsp;Yitian Zhang,&nbsp;Mingzhu Zhou,&nbsp;Hanjiang Gu,&nbsp;Mei Lu,&nbsp;Yumin Xia","doi":"10.1016/j.jdermsci.2024.02.007","DOIUrl":"10.1016/j.jdermsci.2024.02.007","url":null,"abstract":"<div><h3>Background</h3><p>Keratinocyte dysdifferentiation and proinflammatory cytokine production play a central role in psoriatic inflammation. According to recent studies, the Rh family C glycoprotein (RHCG) enhances cell proliferation and disrupts cell differentiation. However, the specific role of RHCG psoriasis development remains unclear.</p></div><div><h3>Objective</h3><p>We here explored the effect of RHCG on keratinocytes under psoriatic inflammation.</p></div><div><h3>Methods</h3><p>The cell counting kit‑8 assay was conducted to assess proliferation. RHCG protein expression was assessed through western blotting and enzyme-linked immunosorbent assays. The expression of proinflammatory cytokines and differentiation markers was analyzed through a quantitative reverse-transcription polymerase chain reaction.</p></div><div><h3>Results</h3><p>Both RHCG mRNA and protein levels increased in psoriatic skin. Notably, cultured keratinocytes treated with an M5 cocktail, which mimics psoriatic inflammation, exhibited higher RHCG expression. Furthermore, RHCG overexpression promoted keratinocyte proliferation, accompanied by an increase in the production of interleukin (IL)-1β, IL-6, and IL-8, and tumor necrosis factor-α. RHCG overexpression also resulted in higher expression of keratin 17, a differentiation marker. Conversely, <em>RHCG</em> gene knockdown reduced keratinocyte proliferation and cytokine secretion. RHCG inhibition in cells recovered both keratin 1 and loricrin expression. Additionally, RHCG overexpression facilitated the phosphorylation of nuclear factor-kappa B and extracellular signal-regulated protein kinase signaling pathways. Importantly, when these signaling pathways were inhibited, the effect of RHCG on keratinocytes was attenuated.</p></div><div><h3>Conclusion</h3><p>These findings support the substantial role of RHCG in psoriatic inflammation development and suggest that RHCG serves as a potential target for psoriasis treatment.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"114 1","pages":"Pages 2-12"},"PeriodicalIF":4.6,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140186668","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":"Editor's Choice","authors":"","doi":"10.1016/S0923-1811(24)00064-1","DOIUrl":"https://doi.org/10.1016/S0923-1811(24)00064-1","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"114 1","pages":"Page 1"},"PeriodicalIF":4.6,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181124000641/pdfft?md5=ce9afcccb3e98cac39366ef4dc6c42cc&pid=1-s2.0-S0923181124000641-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140818357","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}