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Vasoactive Intestinal Peptide Operates as a Negative Regulator of Human Hair Follicle Pigmentation Ex Vivo. 血管活性肠肽(VIP)是人体内毛囊色素沉着的负向调节因子。
Pub Date : 2024-09-07 DOI: 10.1016/j.jid.2024.06.1290
Tatiana Gomez Gomez, Jérémy Chéret, Barbara Bedogni, Ramtin Kassir, Marta Bertolini, Ralf Paus
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引用次数: 0
Invasion of Human Epidermis by Malassezia furfur Is Strain Dependent. 糠秕马拉色菌侵入人体表皮与菌株有关。
Pub Date : 2024-09-07 DOI: 10.1016/j.jid.2024.07.028
Bastien Tirtiaux, Giuseppe Ianiri, Valérie De Glas, Eléa Denil, Emilie Faway, Yves Poumay
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引用次数: 0
Phosphodiesterase-4 Inhibitors Increase Pigment Cell Proliferation and Melanization in Cultured Melanocytes and within a 3-Dimensional Skin Equivalent Model. 磷酸二酯酶-4 抑制剂可增加培养黑色素细胞和三维皮肤等效模型中色素细胞的增殖和黑色素化。
Pub Date : 2024-09-07 DOI: 10.1016/j.jid.2024.08.005
Nathaniel B Goldstein, Zachary B K Berk, Landon C Tomb, Junxiao Hu, Laura G Hoaglin, Dennis R Roop, Roni Adiri, Yonghua Zhuang, Juliana M Canosa, Paul Sanders, David A Norris, Karl Nocka, Amy Cha, Stanca A Birlea

Vitiligo is a common chronic autoimmune disease characterized by white macules and patches of the skin, having a negative impact on patients' life and without any definitive cure at present. Identification of new compounds to reverse depigmentation is therefore a pressing need for this disease. The pharmacologic compounds phosphodiesterase-4 inhibitors (PDE4is) are small molecules with immunomodulatory properties used for treatment of inflammatory dermatoses. PDE4is have shown repigmentation effects in patients with vitiligo, in some case reports. We characterized the proliferative and melanogenic potential of 2 known PDE4is-crisaborole and roflumilast-and of a more recently designed compound, PF-07038124. We used 2 in vitro model systems-the primary human melanocyte culture and a 3-dimensional cocultured skin model (MelanoDerm)-with an exploratory testing platform composed of complementary assays (spectrophotometry, melanin and proliferation assays, immunostaining, Fontana-Masson staining, RT-qPCR, western blot, and whole-transcriptome RNA sequencing). We identified that treatment with PDE4is was associated with increased melanocyte proliferation and melanization in both in vitro models and with increase in the melanogenic genes and proteins expression in cultured melanocytes. These effects were found to be enhanced by addition of α-melanocyte-stimulating hormone. Our findings support the further evaluation of PDE4is with or without α-melanocyte-stimulating hormone agonists in vitiligo trials.

白癜风是一种常见的慢性自身免疫性疾病,其特征是皮肤上出现白色斑丘疹和斑块,对患者的生活造成负面影响,目前还没有任何确切的治疗方法。因此,寻找能逆转脱色的新化合物是这种疾病的迫切需要。药理化合物磷酸二酯酶-4 抑制剂(PDE4i)是一种具有免疫调节特性的小分子化合物,用于治疗炎症性皮肤病。在一些病例报告中,PDE4i 对白癜风患者有色素恢复作用。我们对两种已知的 PDE4i(crisaborole 和 roflumilast)以及最近设计的一种化合物 PF-07038124 的增殖和黑色素生成潜力进行了鉴定。我们使用了两个体外模型系统,即原代人类黑色素细胞培养和三维共培养皮肤模型(MelanoDermTM),以及一个由互补性检测方法(分光光度法、黑色素和增殖检测、免疫染色、Fontana-Masson 染色、qRT-PCR、Western 印迹和全转录组 RNA 序列测定)组成的探索性测试平台。我们发现,在两种体外模型中,PDE4i 的治疗都与黑色素细胞增殖和黑色素化的增加有关,并与培养的黑色素细胞中黑色素生成基因和蛋白表达的增加有关。加入α-MSH后,这些效应都会增强。我们的研究结果支持在白癜风试验中进一步评估加入或不加入α-MSH激动剂的PDE4i。
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引用次数: 0
Tumor RNA Sequencing Identifies a Group of Patients with Mycosis Fungoides with Failure of Skin-Directed Therapies. 肿瘤 RNA 测序确定了一组皮肤导向疗法失败的真菌病患者。
Pub Date : 2024-09-06 DOI: 10.1016/j.jid.2024.06.1292
Marjaana Häyrinen, Hanna-Riikka Teppo, Liisa Väkevä, Annamari Ranki, Henry J Barton, Katja Porvari, Jenni Kiiskilä, Milla E L Kuusisto, Hanne Kuitunen, Siria Lemma, Helka Sahi, Kirsi-Maria Haapasaari, Outi Kuittinen
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引用次数: 0
Heterogeneity in keloid scars: influence of mechanical stretching on keloids arising from different anatomical sites. 瘢痕疙瘩的异质性:机械拉伸对不同解剖部位瘢痕疙瘩的影响。
Pub Date : 2024-09-06 DOI: 10.1016/j.jid.2024.08.016
Young In Lee, Yohan Yang, Seoyoon Ham, Jung Eun Shim, Sang Gyu Lee, Si-Hyung Lee, Tae-Gyun Kim, Won Jai Lee, Do-Young Kim, Ju Hee Lee
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引用次数: 0
Weak Hydrogen Bonds in Temporary Shape Changes of Curly Human Hair Fibers: Preliminary Evidence. 卷曲人发纤维临时形状变化中的弱氢键:初步证据
Pub Date : 2024-09-05 DOI: 10.1016/j.jid.2024.06.1282
Elsabe Cloete, Malebogo N Ngoepe, Ernesto Ismail, Nonhlanhla P Khumalo
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引用次数: 0
The Skin Acid Mantle: An Update on Skin pH. 皮肤酸性外壳:皮肤酸碱度的最新进展。
Pub Date : 2024-09-05 DOI: 10.1016/j.jid.2024.07.009
Sarah G Brooks, Rami H Mahmoud, Rachel R Lin, Joachim W Fluhr, Gil Yosipovitch

The acid mantle concept refers to the buffer system located in the upper stratum corneum of the skin. By sustaining an acidic environment, the acid mantle contributes to the regulation of the microbiome, structural stability, and inflammation. Skin pH is pivotal in maintaining the integrity of the epidermal barrier. Shifts in pH can disrupt barrier properties, and recent studies have emphasized its impact on dermatologic disease processes. This review explores the complex relationship of mechanisms through which skin pH impacts dermatologic pathologies. Furthermore, we highlight the promising potential of pH-targeted therapies for advancing the management of skin conditions.

酸幔概念是指位于皮肤上层角质层的缓冲系统。通过维持酸性环境,酸幔有助于调节微生物群、结构稳定性和炎症。皮肤的 pH 值是维持表皮屏障完整性的关键。pH 值的变化会破坏屏障的特性,最近的研究强调了它对皮肤病过程的影响。本综述探讨了皮肤 pH 值影响皮肤病病理机制的复杂关系。此外,我们还强调了 pH 值靶向疗法在促进皮肤病治疗方面的巨大潜力。
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引用次数: 0
The Pigmentation of Blue Light Is Mediated by Both Melanogenesis Activation and Autophagy Inhibition through OPN3-TRPV1. 蓝光的色素沉着是通过 OPN3-TRPV1 激活黑色素生成和抑制自噬介导的。
Pub Date : 2024-09-04 DOI: 10.1016/j.jid.2024.07.034
Eunbi Yu, Sae Woong Oh, See-Hyoung Park, Kitae Kwon, Su Bin Han, Su Hyun Kang, Jung Hyun Lee, Heejun Ha, Donghoon Yoon, Eunsun Jung, Minkyung Song, Jae Youl Cho, Jongsung Lee

Blue light, a high-energy radiation in the visible light spectrum, was recently reported to induce skin pigmentation. In this study, we investigated the involvement of TRPV1-mediated signaling along with OPN3 in blue light-induced melanogenesis as well as its signaling pathway. Operating downstream target of OPN3 in blue light-induced melanogenesis, blue light activated TRPV1 and upregulated its expression, resulting in calcium influx. Calcium ion induced the activation of calcium/calmodulin-dependent protein kinase II and MAPK. It also downregulated clusterin expression, leading to the nuclear translocation of PAX3, ultimately affecting melanin synthesis. In addition, blue light interfered with autophagy-mediated regulation of melanosomes by decreasing not only the interaction between clusterin and LC3B but the expression of activating transcription factor family. These findings demonstrate that the pigmenting effects of blue light are mediated by calcium/calmodulin-dependent protein kinase II- and MAPK-mediated signaling as well as clusterin-dependent inhibition of autophagy through OPN3-TRPV1-calcium influx, suggesting, to our knowledge, a previously unreported signaling pathway through which blue light regulates melanocyte biology. Furthermore, these results suggest that TRPV1 and clusterin could be potential therapeutic targets for blue light-induced pigmentation due to prolonged exposure to blue light.

蓝光是可见光光谱中的一种高能辐射,最近有报道称它能诱导皮肤色素沉着。在这项研究中,我们研究了TRPV1介导的信号传导与OPN3在蓝光诱导的黑色素生成中的参与及其信号传导途径。OPN3是蓝光诱导黑色素生成的下游靶点,蓝光激活TRPV1并上调其表达,导致钙离子流入。[Ca2+]诱导激活 CaMKII 和 MAPK。它还下调了簇蛋白的表达,导致 PAX3 的核转位,最终影响黑色素的合成。此外,蓝光不仅降低了CLU和LC3B之间的相互作用,还降低了ATF家族的表达,从而干扰了自噬介导的黑色素体调节。这些研究结果表明,蓝光的色素沉着作用是由CaMKII和MAPK介导的信号传导以及CLU通过OPN3-TRPV1-钙离子流入对自噬的依赖性抑制所介导的,这表明蓝光调节黑色素细胞生物学的一个新的信号传导途径。此外,这些结果表明,TRPV1和CLU可能是蓝光诱导的色素沉着的潜在治疗靶点。
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引用次数: 0
NETSKINMODELS: A European Network for Skin Engineering and Modeling. 网络皮肤模型:欧洲皮肤工程和建模网络。
Pub Date : 2024-09-03 DOI: 10.1016/j.jid.2024.03.049
Hristijan Goreski, Dusko Ilic, Vincent Flacher, Ellen van den Bogaard, Christina Guttmann-Gruber, Reiko J Tanaka, Gülcihan Gülseren, Christophe Marquette, Joachim Fluhr, Viviane Filor, Serghei Sprincean, Sandrine Dubrac
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引用次数: 0
Type III Collagen Regulates Matrix Architecture and Mechanosensing during Wound Healing. III 型胶原蛋白在伤口愈合过程中调节基质结构和机械感应。
Pub Date : 2024-09-03 DOI: 10.1016/j.jid.2024.08.013
Daniel C Stewart, Becky K Brisson, William K Yen, Yuchen Liu, Chao Wang, Gordon Ruthel, Donald Gullberg, Robert L Mauck, Malcolm Maden, Lin Han, Susan W Volk

Postnatal cutaneous wound healing is characterized by development of a collagen-rich scar lacking the architecture and functional integrity of unwounded tissue. Directing cell behaviors to efficiently heal wounds while minimizing scar formation remains a major wound management goal. In this study, we demonstrate type III collagen (COL3) as a critical regulator of re-epithelialization and scar formation during healing of COL3-enriched, regenerative (Acomys), scar-permissive (CD-1 Mus and wild-type Col3B6/B6 mice) and COL3-deficient, scar-promoting (Col3F/F, a murine conditional knockdown model) cutaneous wound models. We define a scar-permissive fibrillar collagen architecture signature characterized by elongated and anisotropically aligned collagen fibers that is dose-dependently suppressed by COL3. Furthermore, loss of COL3 alters how cells interpret their microenvironment-their mechanoperception-such that COL3-deficient cells display mechanically active phenotypes in the absence of increased microenvironmental stiffness through the upregulation and engagement of the profibrotic integrin α11. Further understanding COL3's role in regulating matrix architecture and mechanoresponses may inform clinical strategies that harness proregenerative mechanisms.

出生后皮肤伤口愈合的特点是形成富含胶原蛋白的疤痕,缺乏未受伤组织的结构和功能完整性。指导细胞行为以有效愈合伤口,同时尽量减少疤痕的形成,仍然是伤口管理的主要目标。在此,我们证明 III 型胶原蛋白(Col3)是富含 Col3、可再生(Acomys)、允许疤痕(CD-1 Mus 和野生型 Col3B6/B6 小鼠)和 Col3 缺乏、促进疤痕(Col3F/F,一种小鼠条件性基因敲除模型)的皮肤伤口模型愈合过程中再上皮化和疤痕形成的关键调节因子。我们确定了疤痕纤维胶原结构特征,其特点是胶原纤维伸长且各向异性排列,Col3对其有剂量依赖性抑制作用。此外,Col3 的缺失改变了细胞对其微环境的解释--它们的机械感知--这样,在微环境硬度没有增加的情况下,Col3 缺失的细胞会通过上调和参与破坏性整合素 α11,显示出机械活跃的表型。进一步了解 Col3 在调节基质结构和机械反应中的作用,可为利用促进再生机制的临床策略提供依据。
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The Journal of investigative dermatology
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