Journal of dermatological science最新文献

{"title":"Proteomic changes related to actin cytoskeleton function in the skin of vildagliptin-treated mice","authors":"Antti Nätynki ,&nbsp;Nina Kokkonen ,&nbsp;Jussi Tuusa ,&nbsp;Steffen Ohlmeier ,&nbsp;Ulrich Bergmann ,&nbsp;Kaisa Tasanen","doi":"10.1016/j.jdermsci.2024.01.003","DOIUrl":"10.1016/j.jdermsci.2024.01.003","url":null,"abstract":"<div><h3>Background</h3><p>Vildagliptin, a dipeptidyl peptidase-4 inhibitor (DPP-4i) is a widely used type 2 diabetes medication that is associated with an up-to 10-fold increased risk for the development of bullous pemphigoid (BP), an autoimmune skin disease. The mechanism by which vildagliptin promotes the development of BP remains unknown.</p></div><div><h3>Objective</h3><p>To elucidate effects of vildagliptin treatment on the mouse cutaneous proteome.</p></div><div><h3>Methods</h3><p>We analyzed the cutaneous proteome of nondiabetic mice treated for 12 weeks with vildagliptin using label-free shotgun mass spectrometry (MS), two-dimensional difference gel electrophoresis (2D-DIGE), immunohistochemistry, immunoblotting, and quantitative real-time polymerase chain reaction.</p></div><div><h3>Results</h3><p>Although vildagliptin treatment did not cause any clinical signs or histological changes in the skin, separate MS and 2D-DIGE analyses revealed altered cutaneous expression of several proteins, many of which were related to actin cytoskeleton remodeling. Altogether 18 proteins were increased and 40 were decreased in the vildagliptin-treated mouse skin. Both methods revealed increased levels of beta-actin and C-&gt;U-editing enzyme APOBEC2 in vildagliptin-treated mice. However, elevated levels of a specific moesin variant in vildagliptin-treated animals were only detected with 2D-DIGE. Immunohistochemical staining showed altered cutaneous expression of DPP-4, moesin, and galectin-1. The changed proteins detected by MS and 2D-DIGE were linked to actin cytoskeleton remodeling, transport, cell movement and organelle assembly.</p></div><div><h3>Conclusion</h3><p>Vildagliptin treatment alters the cutaneous proteome of nondiabetic mice even without clinical signs in the skin. Cytoskeletal changes in the presence of other triggering factors may provoke a break of immune tolerance and further promote the development of BP.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181124000112/pdfft?md5=fa59a26f8ead77c260c8005b8659af5f&pid=1-s2.0-S0923181124000112-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139515231","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)00044-6","DOIUrl":"https://doi.org/10.1016/S0923-1811(24)00044-6","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181124000446/pdfft?md5=b701227dd1c6ce7af31e062082e5aa5a&pid=1-s2.0-S0923181124000446-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140543685","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":"Acquired curved hair is caused by fusion of multiple hair matrix cells","authors":"Ippei Horibe ,&nbsp;Sara Izumi ,&nbsp;Yuru Ke ,&nbsp;Nanami Tanahashi ,&nbsp;Yusuke Takagi ,&nbsp;Ryoji Ishihara ,&nbsp;Takaya Nakano ,&nbsp;Takaaki Sumiyoshi ,&nbsp;Yasuo Nagaoka","doi":"10.1016/j.jdermsci.2024.02.002","DOIUrl":"10.1016/j.jdermsci.2024.02.002","url":null,"abstract":"<div><h3>Background</h3><p>“Curved hair” caused by acquired factors is considered to have adverse cosmetic effects, but the detailed mechanism behind curved hair remains obscure.</p></div><div><h3>Objective</h3><p>We attempted to clarify the causes of curved hair that appeared to have occurred via acquired factors.</p></div><div><h3>Methods</h3><p>Outer root sheath cells (ORSC) isolated from plucked human hair follicles were used to evaluate the expression of type IV collagen. Straight and curved hairs with hair follicle tissue attached were also collected from the same individuals and subjected to morphological, immunohistochemical, and gene expression analyses.</p></div><div><h3>Results</h3><p>The amount of type IV collagen increased upon inducing endoplasmic reticulum stress in ORSC. Meanwhile, in curved hair follicle tissue, the gene expression of type IV collagen decreased. In addition, the curved hair follicle tissue obtained from participants in their 30 s to 50 s had distorted shapes compared with that of straight hair from the same individuals. It was also observed that hair matrix cells based on multiple hair germs fused to eventually form a single hair follicle and hair shaft. In curved hair follicle tissue, KRT71 protein, a marker of inner root sheath differentiation, was unevenly distributed and there was elevated expression of Dickkopf-1 (DKK1) protein, an inhibitor of the Wnt signaling pathway.</p></div><div><h3>Conclusion</h3><p>Our study revealed the fusion of hair matrix cells during hair follicle regeneration as a cause of acquired curved hair. We consider that such fusion causes hair follicle tissue to abnormally differentiate, resulting in asymmetric hair follicle shapes and curved hair.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139827548","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":"Combined effect of Neurotropin® and methylcobalamin on postherpetic neuralgia in mice infected with herpes simplex virus type-1","authors":"Tsugunobu Andoh ,&nbsp;Takashi Kikukawa ,&nbsp;Atsushi Kotani ,&nbsp;Yoko Kurokawa ,&nbsp;Wakana Asakura ,&nbsp;Kengo Houmoto ,&nbsp;Daisuke Fukutomi ,&nbsp;Daisuke Uta ,&nbsp;Hisashi Okai ,&nbsp;Koji Koike","doi":"10.1016/j.jdermsci.2024.02.004","DOIUrl":"10.1016/j.jdermsci.2024.02.004","url":null,"abstract":"<div><h3>Background</h3><p>Postherpetic pain (PHP) is difficult to control. Although Neurotropin® (NTP) and methylcobalamin (MCB) are often prescribed to treat the pain, the efficacy of combined treatment for PHP remains imcompletely understood.</p></div><div><h3>Objective</h3><p>In this study, we investigate the combined effects of NTP and MCB on PHP in mice.</p></div><div><h3>Methods</h3><p>NTP and MCB were administered from day 10–29 after herpes simplex virus type-1 (HSV-1) infection. The pain-related responses were evaluated using a paint brush. The expression of neuropathy-related factor (ATF3) and nerve repair factors (GAP-43 and SPRR1A) in the dorsal root ganglion (DRG) and neurons in the skin were evaluated by immunohistochemical staining. Nerve growth factor (NGF) and neurotrophin-3 (NT3) mRNA expression levels were evaluated using real-time PCR.</p></div><div><h3>Results</h3><p>Repeated treatment with NTP and MCB after the acute phase inhibited PHP. Combined treatment with these drugs inhibited PHP at an earlier stage than either treatment alone. In the DRG of HSV-1-infected mice, MCB, but not NTP, decreased the number of cells expressing ATF3 and increased the number of cells expressing GAP-43- and SPRR1A. In addition, MCB, but not NTP, also increased and recovered non-myelinated neurons decreased in the lesional skin. NTP increased the mRNA levels of NTF3 in keratinocytes, while MCB increased that of NGF in Schwann cells.</p></div><div><h3>Conclusion</h3><p>These results suggest that combined treatment with NTP and MCB is useful for the treatment of PHP. The combined effect may be attributed to the different analgesic mechanisms of these drugs.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139886023","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 GRHL3-regulated long non-coding RNA lnc-DC modulates keratinocytes differentiation by interacting with IGF2BP2 and up-regulating ZNF750","authors":"Xue-ting Hu ,&nbsp;Xiao-feng Wu ,&nbsp;Lu-min Sui ,&nbsp;Luo-quan Ao ,&nbsp;Cheng-xiu Pu ,&nbsp;Mu Yuan ,&nbsp;Wei Xing ,&nbsp;Xiang Xu","doi":"10.1016/j.jdermsci.2024.02.003","DOIUrl":"10.1016/j.jdermsci.2024.02.003","url":null,"abstract":"<div><h3>Background</h3><p>Aberrant keratinocytes differentiation has been demonstrated to be associated with a number of skin diseases. The roles of lncRNAs in keratinocytes differentiation remain to be largely unknown.</p></div><div><h3>Objective</h3><p>Here we aim to investigate the role of lnc-DC in regulating epidermal keratinocytes differentiation.</p></div><div><h3>Methods</h3><p>Expression of lnc-DC in the skin was queried in AnnoLnc and verified by FISH. The lncRNA expression profiles during keratinocytes differentiation were reanalyzed and verified by qPCR and FISH. Gene knock-down and over-expression were used to explore the role of lnc-DC in keratinocytes differentiation. The downstream target of lnc-DC was screened by whole transcriptome sequencing. CUT&amp;RUN assay and siRNAs transfection was used to reveal the regulatory effect of GRHL3 on lnc-DC. The mechanism of lnc-DC regulating ZNF750 was revealed by RIP assay and RNA stability assay.</p></div><div><h3>Results</h3><p>Lnc-DC was biasedly expressed in skin and up-regulated during epidermal keratinocytes differentiation. Knockdown lnc-DC repressed epidermal keratinocytes differentiation while over-express lnc-DC showed the opposite effect. GRHL3, a well-known transcription factor regulating keratinocytes differentiation, could bind to the promoter of lnc-DC and regulate its expression. By whole transcriptome sequencing, we identified that ZNF750 was a downstream target of lnc-DC during keratinocytes differentiation. Mechanistically, lnc-DC interacted with RNA binding protein IGF2BP2 to stabilize ZNF750 mRNA and up- regulated its downstream targets TINCR and KLF4.</p></div><div><h3>Conclusion</h3><p>Our study revealed the novel role of GRHL3/lnc-DC/ZNF750 axis in regulating epidermal keratinocytes differentiation, which may provide new therapeutic targets of aberrant keratinocytes differentiation related skin diseases.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139887385","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":"JAK inhibitors for the treatment of vitiligo","authors":"Shintaro Inoue ,&nbsp;Tamio Suzuki ,&nbsp;Shigetoshi Sano ,&nbsp;Ichiro Katayama","doi":"10.1016/j.jdermsci.2023.12.008","DOIUrl":"10.1016/j.jdermsci.2023.12.008","url":null,"abstract":"<div><p>Vitiligo<span><span> is an autoimmune disease involving melanocyte-targeting T cells initiated by environmental and </span>genetic factors<span><span><span><span>. Steroids and tacrolimus have been used as topical treatments. Recently, novel </span>topical agents<span> targeting Janus kinase (JAK), a family of </span></span>tyrosine kinases<span><span> that regulates cytokine signaling, have emerged. </span>Ruxolitinib<span> is the first approved in vitiligo therapy. Furthermore, ritlecitinib is currently under </span></span></span>clinical trials<span> for oral treatment of active vitiligo. In this review, we discuss the possibility of topical JAK inhibitors as promising options for the treatment of vitiligo with regard to their mechanism of action, efficacy and safety.</span></span></span></p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139421452","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":"Decreased TET2/5-hmC reduces the integrity of the epidermal barrier via epigenetic dysregulation of filaggrin in psoriatic lesions","authors":"Huan Zhang ,&nbsp;Tao Jia ,&nbsp;Delu Che ,&nbsp;Bin Peng ,&nbsp;Zhaowei Chu ,&nbsp;Xiangjin Song ,&nbsp;Weihui Zeng ,&nbsp;Songmei Geng","doi":"10.1016/j.jdermsci.2024.01.004","DOIUrl":"10.1016/j.jdermsci.2024.01.004","url":null,"abstract":"<div><h3>Background</h3><p><span>TET2 participates in tumor progression and intrinsic immune homeostasis via </span>epigenetic<span> regulation. TET2 has been reported to be involved in maintaining epithelial barrier homeostasis and inflammation. Abnormal epidermal barrier function and TET2 expression have been detected in psoriatic lesions. However, the mechanisms underlying the role of TET2 in psoriasis have not yet been elucidated.</span></p></div><div><h3>Objective</h3><p>To define the role of TET2 in maintaining epithelial barrier homeostasis and the exact epigenetic mechanism in the dysfunction of the epidermal barrier in psoriasis.</p></div><div><h3>Methods</h3><p><span><span><span>We analyzed human psoriatic skin lesions and datasets from the </span>GEO database, and detected the expression of TET2/5-hmC together with barrier molecules by </span>immunohistochemistry<span>. We constructed epidermal-specific TET2 knockout mice to observe the effect of TET2 deficiency on epidermal barrier function via toluidine blue penetration assay. Further, we analyzed changes in the expression of epidermal barrier molecules by </span></span>immunofluorescence in TET2-specific knockout mice and psoriatic model mice.</p></div><div><h3>Results</h3><p><span><span><span>We found that decreased expression of TET2/5-hmC correlated with dysregulated barrier molecules in human psoriatic lesions. Epidermal-specific TET2 knockout mice showed elevated transdermal </span>water loss associated with abnormal epidermal barrier molecules. Furthermore, we observed that TET2 knockdown in </span>keratinocytes reduced </span>filaggrin<span> expression via filaggrin promoter methylation.</span></p></div><div><h3>Conclusion</h3><p>Aberrant epidermal TET2 affects the integrity of the epidermal barrier through the epigenetic dysregulation of epidermal barrier molecules, particularly filaggrin. Reduced TET2 expression is a critical factor contributing to an abnormal epidermal barrier in psoriasis.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139514955","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":"Mass spectrometry -based proteomic analysis of the skin of patients with localized scleroderma","authors":"Katariina Mähönen ,&nbsp;Salla Keskitalo ,&nbsp;Kari Salokas ,&nbsp;Antti Tuhkala ,&nbsp;Jaana Panelius ,&nbsp;Annamari Ranki ,&nbsp;Markku Varjosalo","doi":"10.1016/j.jdermsci.2024.01.005","DOIUrl":"10.1016/j.jdermsci.2024.01.005","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181124000136/pdfft?md5=dea3389dbf90a87d558871df85d1201c&pid=1-s2.0-S0923181124000136-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139554153","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 Staphylococcus epidermidis strain inhibits the uptake of Staphylococcus aureus derived from atopic dermatitis skin into the keratinocytes","authors":"Tomofumi Numata,&nbsp;Kazumasa Iwamoto,&nbsp;Kyouka Matsunae,&nbsp;Ryu Miyake,&nbsp;Masataka Suehiro,&nbsp;Nozomi Yanagida,&nbsp;Takanobu Kan,&nbsp;Shunsuke Takahagi,&nbsp;Michihiro Hide,&nbsp;Akio Tanaka","doi":"10.1016/j.jdermsci.2024.01.006","DOIUrl":"10.1016/j.jdermsci.2024.01.006","url":null,"abstract":"<div><h3>Background</h3><p>Various bacterial species form a microbiome in the skin. In the past, dead <em>Staphylococcus aureus</em> derived from atopic dermatitis (AD) are taken up by keratinocytes; however, whether live <em>S. aureus</em> can be taken up by keratinocytes is unknown.</p></div><div><h3>Objective</h3><p>This study aimed to examine whether live AD strains of <em>S. aureus</em> internalize into the keratinocytes and how the internalization changes under conditions in which other bacterial species including <em>S. epidermidis</em> are present.</p></div><div><h3>Methods</h3><p>HaCaT cells were cultured with live <em>S. aureus</em> and <em>S. epidermidis</em> (live or heat-treated) or their culture supernatants. After coculture, the change in the amount of <em>S. aureus</em> in the cytoplasm of HaCaT cells was analyzed using, a high-throughput imaging system, Opera Phenix™.</p></div><div><h3>Results</h3><p>Live <em>S. aureus</em> were taken up in the cytoplasm of HaCaT cells. Coculturing live <em>S. aureus</em> with live <em>S. epidermidis</em> or the culture supernatants decreased the abundance of <em>S. aureus</em> in the cytoplasm. The heat-treated culture supernatants of live <em>S. epidermidis</em> or culture supernatants of other <em>S.</em> strains did not decrease the abundance of <em>S. aureus</em> in the cytoplasm.</p></div><div><h3>Conclusion</h3><p>Live <em>S. aureus</em> was internalized into the cytoplasm of HaCaT cells as does heat-treated <em>S. aureus</em>. In addition, the heat-sensitive substances secreted by coculture with <em>S. epidermidis</em> and keratinocytes inhibited the uptake of <em>S. aureus</em> by keratinocytes.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139648783","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":"Interleukin-36γ/interleukin-37 ratio in the stratum corneum correlates with facial redness","authors":"Tetsuya Kuwano,&nbsp;Takatoshi Murase","doi":"10.1016/j.jdermsci.2023.12.001","DOIUrl":"10.1016/j.jdermsci.2023.12.001","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138555442","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}