Journal of dermatological science最新文献

英文中文

Senescent fibroblasts and innate immune cell activation might play a role in the pathogenesis of elderly atopic dermatitis 衰老成纤维细胞和先天性免疫细胞活化可能在老年特应性皮炎的发病机制中发挥作用

IF 4.6

Journal of dermatological science

Pub Date : 2024-06-01 DOI: 10.1016/j.jdermsci.2024.04.002

Yang Luo , Xiaokai Fang , Yuan Zhou , Yu Zhang , Wei Li , Sean X. Leng , Xu Yao , Xiaochun Liu

Background

Elderly atopic dermatitis (AD) is a subtype of AD defined by age (≥ 60 years). The molecular characteristics of elderly AD remain to be clarified.

Objective

We sought to characterize the molecular features of skin lesions and peripheral blood mononuclear cells (PBMCs) in patients with AD across different age, focusing on elderly AD.

Methods

Skin and PBMCs samples were used for RNA sequencing. Analysis of differentially expressed genes and gene set variation analysis were performed. Immunofluorescence staining, quantitative real-time PCR (qRT-PCR), flow cytometry and transwell assay were used for validation.

Results

Compared with healthy controls, the skin transcriptome of AD patients showed common signatures of AD, like barrier dysfunction and enhanced Th1/Th2/Th17 immune pathways. In PBMCs, the expression of Th1/Th2 response genes was more remarkable in adult AD, while expression of Th17-related genes was significantly higher in childhood AD. The gene modules associated with natural killer (NK) cells were downregulated in elderly AD. In skin lesions, elderly AD exhibited enrichment of macrophages, fibroblasts and senescence-associated secretory phenotype (SASP) related genes. The correlation among fibroblasts, SASP and innate immune cells were revealed by the co-localization of fibroblasts, macrophages and NK cells in the lesions across different age groups. Fibroblasts under inflammation or senescence could induce stronger chemotaxis of macrophages and NK cells.

Conclusion

We identified the molecular phenotypes of skin lesions and PBMCs in elderly AD individuals. Fibroblasts, innate immune cells, and SASP might play important roles in the pathogenesis of elderly AD.

背景老年特应性皮炎（AD）是根据年龄（≥ 60 岁）定义的 AD 亚型。我们试图研究不同年龄段特应性皮炎患者皮肤病变和外周血单核细胞（PBMCs）的分子特征，重点研究老年特应性皮炎。方法对皮肤和 PBMCs 样品进行 RNA 测序，并进行差异表达基因分析和基因组变异分析。结果与健康对照组相比，AD 患者皮肤转录组显示出 AD 的共同特征，如屏障功能障碍和 Th1/Th2/Th17 免疫通路增强。在PBMCs中，Th1/Th2反应基因的表达在成人AD中更为显著，而Th17相关基因的表达在儿童AD中明显升高。与自然杀伤（NK）细胞相关的基因模块在老年 AD 中下调。在皮肤病变中，老年 AD 表现出巨噬细胞、成纤维细胞和衰老相关分泌表型（SASP）相关基因的富集。成纤维细胞、SASP和先天性免疫细胞之间的相关性通过成纤维细胞、巨噬细胞和NK细胞在不同年龄组皮损中的共定位而得以揭示。炎症或衰老状态下的成纤维细胞可诱导巨噬细胞和 NK 细胞产生更强的趋化性。成纤维细胞、先天性免疫细胞和 SASP 可能在老年 AD 的发病机制中发挥重要作用。

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引用次数: 0

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IF 4.6

Journal of dermatological science

Pub Date : 2024-06-01 DOI: 10.1016/S0923-1811(24)00118-X

引用次数: 0

FTO-mediated regulation of m6A methylation is closely related to apoptosis induced by repeated UV irradiation FTO 介导的 m6A 甲基化调控与反复紫外线照射诱导的细胞凋亡密切相关

IF 4.6

Journal of dermatological science

Pub Date : 2024-06-01 DOI: 10.1016/j.jdermsci.2024.01.001

Yao Lin , Yu Sun , Wenyi Hou , Xinling Chen , Feng Zhou , QingFang Xu , Yue Zheng

Background

Ultraviolet (UV) damage is closely related to skin photoaging and many skin diseases, including dermatic tumors. N6-methyladenosine (m6A) modification is an important epigenetic regulatory mechanism. However, the role of m6A methylation in apoptosis induced by repeated UV irradiation has not been characterized.

Objective

To explore m6A methylation changes and regulatory mechanisms in the repeated UV-induced skin damage process, especially apoptosis.

Methods

HaCaT cells and BALB/c-Nu nude mice were exposed to repeated UVB/UVA+UVB irradiation. Colorimetry and flow cytometry were used to measure cellular viability and apoptosis. m6A-modified genes were detected via colorimetry and methylated RNA immunoprecipitation (MeRIP) sequencing. Methyltransferases and demethylases were detected via RT-PCR, western blotting and immunohistochemistry. Transfection of siRNA and plasmid was performed to knock down or overexpress the selected genes.

Results

After UVB irradiation, 861 m6A peaks were increased and 425 m6A peaks were decreased in HaCaT cells. The differentially modified genes were enriched in apoptosis-related pathways. The m6A demethylase FTO was decreased in both HaCaT cells and mouse skin after UV damage. Overexpressing FTO could improve cell viability, inhibit apoptosis and decrease RNA-m6A methylation, including LPCAT3-m6A, which increase LPCAT3 expression, cell viability promotion and apoptosis inhibition.

Conclusion

Our study identified the cell m6A methylation change lists after repeated UVB irradiation, and revealed that FTO and LPCAT3 play key roles in the m6A methylation pathogenesis of UV-induced skin cell apoptosis. FTO-m6A-LPCAT3 might serve as a novel upstream target for preventing and treating photoaging and UV-induced skin diseases.

背景紫外线（UV）损伤与皮肤光老化和许多皮肤病（包括皮肤肿瘤）密切相关。N6-甲基腺苷（m6A）修饰是一种重要的表观遗传调控机制。目的探讨 m6A 甲基化在反复紫外线照射诱导的皮肤损伤过程（尤其是细胞凋亡）中的变化和调控机制。方法将 HaCaT 细胞和 BALB/c-Nu 裸鼠暴露于反复 UVB/UVA+UVB 照射。通过比色法和甲基化 RNA 免疫沉淀（MeRIP）测序检测 m6A 修饰基因。通过 RT-PCR、Western 印迹和免疫组织化学检测甲基转移酶和去甲基化酶。结果UVB照射后，HaCaT细胞中有861个m6A峰增加，425个m6A峰减少。差异修饰的基因富集在与细胞凋亡相关的通路中。紫外线损伤后，HaCaT 细胞和小鼠皮肤中的 m6A 去甲基化酶 FTO 都减少了。结论我们的研究确定了反复紫外线照射后细胞 m6A 甲基化变化列表，并揭示了 FTO 和 LPCAT3 在紫外线诱导皮肤细胞凋亡的 m6A 甲基化发病机制中起关键作用。FTO-m6A-LPCAT3可能是预防和治疗光老化和紫外线诱导的皮肤病的一个新的上游靶点。

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引用次数: 0

Oxidative stress-induced hypermethylation and low expression of ANXA2R: Novel insights into the dysfunction of melanocytes in vitiligo 氧化应激诱导的高甲基化和ANXA2R的低表达：对白癜风黑色素细胞功能障碍的新认识

IF 4.6

Journal of dermatological science

Pub Date : 2024-06-01 DOI: 10.1016/j.jdermsci.2024.02.009

Jiaxi Chen, Yinghan Wang, Wei Dai, Xinyuan Xu, Qingrong Ni , Xiuli Yi, Pan Kang, Jingjing Ma, Lili Wu, Chunying Li, Shuli Li

Background

Vitiligo is a skin disorder with melanocyte destruction caused by complex interplay between multiple genetic and environmental factors. Recent studies have suggested DNA methylation is involved in the melanocyte damage, but the underlying mechanism remains unknown.

Objective

To explore the abnormal DNA methylation patterns in vitiligo lesional and nonlesional skin, and the mechanism of DNA methylation involved in vitiligo pathogenesis.

Methods

Initially, the genome-wide aberrant DNA methylation profiles in lesional and nonlesional skin of vitiligo were detect via Illumina methylation EPIC 850k Beadchip. Subsequently, a comprehensive analysis was conduct to investigate the genomic characteristics of differentially methylated regions (DMRs). Furthermore, the effects of key aberrant methylated genes on cell apoptosis and function of both melanocytes and keratinocytes were further identified and validated by western bloting, ELISA, and immunofluorescence.

Results

Compared with nonlesional skins, we discovered 79 significantly differentially methylated CpG sites in vitiligo lesions. These DMRs were mainly located in the gene body and the TS1500 region. Annexin A2 receptor (ANXA2R), a crucial gene in cell apoptosis, was hypermethylated in vitiligo lesions. Furthermore, we showed that ANXA2R displayed hypermethylation and low expression levels in both keratinocytes and melanocytes of vitiligo patients, and the hypermethylated-triggered downregulation of ANXA2R under oxidative stress induced melanocyte apoptosis, and inhibited the secretion of stem cell factor (SCF) from keratinocytes thus impaired the survival of melanocytes.

Conclusions

Our study illustrates the DNA methylation modiﬁcation in vitiligo, and further demonstrates the molecular mechanism of hypermethylated ANXA2R in the dysfunction of melanocytes under oxidative stress.

背景白癜风是一种由多种遗传和环境因素复杂相互作用引起的黑素细胞破坏性皮肤病。方法首先，通过Illumina甲基化EPIC 850k Beadchip检测白癜风皮损和非皮损皮肤全基因组DNA甲基化异常图谱。随后，对差异甲基化区域（DMRs）的基因组特征进行了综合分析。结果与非皮损性皮肤相比，我们在白癜风皮损中发现了 79 个具有显著差异的 CpG 甲基化位点。这些DMRs主要位于基因体和TS1500区域。Annexin A2受体（ANXA2R）是细胞凋亡的关键基因，在白癜风皮损中出现了高甲基化。此外，我们还发现，ANXA2R在白癜风患者的角朊细胞和黑素细胞中均表现出高甲基化和低表达水平，在氧化应激作用下，ANXA2R的高甲基化触发下调诱导黑素细胞凋亡，并抑制角朊细胞分泌干细胞因子（SCF），从而损害黑素细胞的存活。结论我们的研究说明了白癜风中的DNA甲基化修饰，并进一步证明了氧化应激下高甲基化ANXA2R导致黑素细胞功能障碍的分子机制。

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引用次数: 0

Mucopolysaccharide polysulfate increases local skin blood volume through nitric oxide production 多硫酸粘多糖通过产生一氧化氮增加局部皮肤血容量

IF 4.6

Journal of dermatological science

Pub Date : 2024-06-01 DOI: 10.1016/j.jdermsci.2024.05.001

Tam Kurachi, Hironobu Ishimaru, Ryo Tadakuma, Miu Okaue, Akira Koda, Yuhki Ueda, Takaaki Doi

Background

Mucopolysaccharide polysulfate (MPS) is widely used as an active ingredient in topical preparations for the treatment of asteatosis and blood flow disorders. Although topical MPS products can increase cutaneous blood flow (CBF), the underlying mechanism remains unclear.

Objective

In this study, we aimed to elucidate how MPS increases CBF. We investigated the association of nitric oxide (NO), a powerful mediator associated with increased local blood volume, with the blood flow-accelerating action of MPS in mice. In addition, we verified the effects of MPS on NO production in different skin cell types, such as keratinocytes (KCs), endothelial cells (ECs), and dermal fibroblasts (DFs).

Methods

We used raster-scanning optoacoustic imaging mesoscopy to observe in vivo changes in the skin blood volume. NO production was determined in each cell using an NO indicator. An enzyme-linked immunoassay was used to measure the phosphorylated nitric oxide synthase (NOS) levels in ECs, DFs, and KCs in the presence or absence of MPS.

Results

Topical application of MPS increased the skin blood volume in mice, and this increase was abolished through the addition of NOS inhibitors. MPS promoted the dose-dependent production of NO in various cells, which caused alterations in the phosphorylation state of NOS.

Conclusion

Our findings demonstrate that MPS promotes an increase in skin blood volume and NO production in various skin cell types. These results suggest that MPS can potentially accelerate CBF through the NO biosynthesis pathway in different skin cell types.

背景多硫酸粘多糖（MPS）作为一种活性成分被广泛应用于治疗骨质疏松症和血流障碍的外用制剂中。虽然外用 MPS 产品可以增加皮肤血流量（CBF），但其基本机制仍不清楚。我们研究了一氧化氮（NO）（一种与局部血容量增加有关的强效介质）与 MPS 对小鼠血流加速作用的关联。此外，我们还验证了 MPS 对角质形成细胞 (KC)、内皮细胞 (EC) 和真皮成纤维细胞 (DF) 等不同类型皮肤细胞中 NO 生成的影响。使用 NO 指示剂测定每个细胞的 NO 产量。结果局部应用 MPS 增加了小鼠的皮肤血容量，通过添加 NOS 抑制剂，这种增加被取消。结论我们的研究结果表明，MPS 能促进皮肤血容量的增加和各种皮肤细胞中 NO 的产生。这些结果表明，MPS 有可能通过不同类型皮肤细胞中的 NO 生物合成途径加速 CBF。

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引用次数: 0

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IF 4.6

Journal of dermatological science

Pub Date : 2024-05-01 DOI: 10.1016/S0923-1811(24)00093-8

引用次数: 0

Anti-BP230 IgE autoantibodies in bullous pemphigoid intraindividually correlate with disease activity 大疱性类天疱疮患者体内的抗 BP230 IgE 自身抗体与疾病活动性有关

IF 4.6

Journal of dermatological science

Pub Date : 2024-05-01 DOI: 10.1016/j.jdermsci.2024.03.009

Shirin Emtenani , Beke E. Linnemann , Andreas Recke , Anabelle von Georg , Stephanie Goletz , Enno Schmidt , Nina van Beek

Background

Bullous pemphigoid (BP), the most common subepidermal autoimmune blistering disease, is classically defined by the presence of IgG autoantibodies directed against the hemidesmosomal proteins BP180 (type XVII collagen) and BP230 and the predominance of skin lesions. Several studies have addressed the role of anti-BP180 IgE in patients and experimental models, while data on anti-BP230 IgE are scarce.

Objective

To assess anti-BP230 IgE level by ELISA in BP sera and to correlate it with disease severity and clinical characteristics.

Methods

BP sera underwent anti-BP230 IgE ELISA and Western blotting against human BP230 fragments.

Results

We demonstrate that 36/154 (23%) of BP sera were positive for anti-BP230 IgE. Anti-BP230 IgE levels had no correlation with clinical phenotype or disease activity per se. Interestingly, anti-BP230 IgE was significantly associated with disease activity within individuals during the course of the disease. Additionally, anti-BP230 IgE and total IgE levels showed a significant correlation. Notably, anti-BP230 IgG correlated interindividually with disease activity. By Western blotting, the C-terminal domain of BP230 fragments (C2; amino acids 2024–2349 and C3; amino acids 2326–2649), provided the best serological assay for anti-BP230 IgE detection.

Conclusion

As a complementary tool, IgE immunoblotting is recommended to obtain an optimal serological diagnosis, particularly in patients with severe disease without IgG reactivity by BP180- or BP230-specific ELISA. Although the detection of serum anti-BP230 IgE is not of major diagnostic significance, it may be relevant for therapeutic decisions, e.g., for anti-IgE-directed treatment, which has been successfully used in case series of BP.

背景大疱性类天疱疮（Bullous pemphigoid，BP）是最常见的表皮下自身免疫性大疱性疾病，其经典定义是存在针对半侧体蛋白 BP180（XVII 型胶原）和 BP230 的 IgG 自身抗体，并且以皮损为主。一些研究探讨了抗 BP180 IgE 在患者和实验模型中的作用，但有关抗 BP230 IgE 的数据却很少。结果我们发现，36/154（23%）份 BP 血清中的抗 BP230 IgE 呈阳性。抗 BP230 IgE 水平与临床表型或疾病活动本身无关。有趣的是，抗 BP230 IgE 与疾病过程中个体的疾病活动性显著相关。此外，抗 BP230 IgE 与总 IgE 水平也有显著相关性。值得注意的是，抗 BP230 IgG 与疾病活动性存在个体间相关性。通过 Western 印迹法，BP230 片段的 C 端结构域（C2；氨基酸 2024-2349 和 C3；氨基酸 2326-2649）为抗 BP230 IgE 检测提供了最佳血清学检测方法。虽然检测血清中的抗 BP230 IgE 并不具有重要的诊断意义，但它可能与治疗决策有关，例如，抗 IgE 引导的治疗，这已成功应用于 BP 的病例系列中。

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