Journal of dermatological science最新文献

英文中文

Scratching, not dryness, drives key skin changes in the AEW-induced dry skin pruritus model, highlighting the importance of breaking itch-scratch cycle in chronic pruritus 在aew诱导的干性皮肤瘙痒模型中，驱动关键皮肤变化的是抓挠，而不是干燥，这突出了在慢性瘙痒中打破痒-抓循环的重要性。

IF 4.6

Journal of dermatological science

Pub Date : 2025-04-09 DOI: 10.1016/j.jdermsci.2025.04.004

Atsuko Funakoshi , Tetsuya Honda

引用次数: 0

Algae ferment regulates initiation, amplification, and resolution of inflammation 藻类发酵调节炎症的发生、扩大和消退。

IF 4.6

Journal of dermatological science

Pub Date : 2025-04-09 DOI: 10.1016/j.jdermsci.2025.04.005

Jaime Emmetsberger , Donald Collins , Nevena Karaman-Jurukovska , Amanda Messina , Dawn Layman , Thomas Mammone , Kenji Kabashima , Nadine Pernodet

引用次数: 0

RN7SL1 overexpression promotes cell proliferation in cutaneous T-cell lymphoma via miR-34a-5p/MYCN axis RN7SL1 过表达通过 miR-34a-5p/MYCN 轴促进皮肤 T 细胞淋巴瘤的细胞增殖。

IF 4.6

Journal of dermatological science

Pub Date : 2025-04-01 DOI: 10.1016/j.jdermsci.2025.03.003

Tingting Li , Jiachen Sun , Guanyu Wang , Yimeng Wang , Chunlei Zhang

Background

Cutaneous T-cell lymphoma (CTCL) is a type of lymphoma that presents in skin tissue without evidence of extracutaneous disease. Emerging evidence indicates that long noncoding RNA-RN7SL1 serves as crucial effectors in modulating progression of different malignancies, including breast cancer, liver cancer, and other neoplasms.

Objective

To figure out the role of RN7SL1 in the pathogenesis of CTCL.

Methods

We detected RN7SL1 expression of CTCL patients by quantitative real-time polymerase chain reaction and fluorescent in situ hybridization. CTCL cell lines were transfected with lentiviral-based RN7SL1 gene knockdown vectors. Whole transcriptome sequencing was conducted to investigate differentially expressed miRNA and mRNA in CTCL, and we used qRT-PCR, RNA immunoprecipitation, dual-luciferase assay, RNA pull down and Western Blotting to further detect the relation of miRNA and mRNA. Also, we have verified above results in mice and clinical samples.

Results

LncRNA-RN7SL1 was overexpressed in CTCL compared with benign inflammatory dermatosis and was related to the TNMB stage of mycosis fungoides and Sézary syndrome (higher expression in IIB-IVB stage than IA-IIA stage). Additionally, the proliferation of CTCL cell lines HH and Hut78 was weakened, but apoptosis was facilitated by RN7SL1 downregulation, resulting in a reduced tumorigenic capacity in vivo. Subsequently, Whole transcriptome sequencing and target validation indicated that the RN7SL1/miR-34a-5p/MYCN axis may promoted malignant behavior in CTCL.

Conclusion

Our study suggested that RN7SL1 promoted malignant behavior by targeting miR-34a-5p/MYCN signaling. This finding might facilitate the discovery of novel biomarkers for CTCL diagnosis and treatment.

背景：皮肤t细胞淋巴瘤（CTCL）是一种表现于皮肤组织而无皮外病变证据的淋巴瘤。越来越多的证据表明，长链非编码RNA-RN7SL1在调节不同恶性肿瘤（包括乳腺癌、肝癌和其他肿瘤）的进展中起着至关重要的作用。目的：探讨RN7SL1在CTCL发病机制中的作用。方法：采用实时定量聚合酶链反应和荧光原位杂交技术检测CTCL患者RN7SL1的表达。用基于慢病毒的RN7SL1基因敲低载体转染CTCL细胞系。通过全转录组测序研究CTCL中miRNA和mRNA的差异表达，并采用qRT-PCR、RNA免疫沉淀、双荧光素酶测定、RNA pull down和Western Blotting进一步检测miRNA和mRNA的关系。我们也在小鼠和临床样本中验证了上述结果。结果：与良性炎性皮肤病相比，LncRNA-RN7SL1在CTCL中过表达，且与蕈样真菌病和ssamzary综合征TNMB分期相关（IIB-IVB期表达高于IA-IIA期表达）。此外，CTCL HH和Hut78细胞系的增殖能力减弱，但RN7SL1下调促进了细胞凋亡，导致体内致瘤能力降低。随后，全转录组测序和靶标验证表明，RN7SL1/miR-34a-5p/MYCN轴可能促进CTCL的恶性行为。结论：我们的研究表明RN7SL1通过靶向miR-34a-5p/MYCN信号通路促进恶性行为。这一发现可能有助于发现新的CTCL诊断和治疗生物标志物。

{"title":"RN7SL1 overexpression promotes cell proliferation in cutaneous T-cell lymphoma via miR-34a-5p/MYCN axis","authors":"Tingting Li , Jiachen Sun , Guanyu Wang , Yimeng Wang , Chunlei Zhang","doi":"10.1016/j.jdermsci.2025.03.003","DOIUrl":"10.1016/j.jdermsci.2025.03.003","url":null,"abstract":"<div><h3>Background</h3><div>Cutaneous T-cell lymphoma (CTCL) is a type of lymphoma that presents in skin tissue without evidence of extracutaneous disease. Emerging evidence indicates that long noncoding RNA-RN7SL1 serves as crucial effectors in modulating progression of different malignancies, including breast cancer, liver cancer, and other neoplasms.</div></div><div><h3>Objective</h3><div>To figure out the role of RN7SL1 in the pathogenesis of CTCL.</div></div><div><h3>Methods</h3><div>We detected RN7SL1 expression of CTCL patients by quantitative real-time polymerase chain reaction and fluorescent in situ hybridization. CTCL cell lines were transfected with lentiviral-based RN7SL1 gene knockdown vectors. Whole transcriptome sequencing was conducted to investigate differentially expressed miRNA and mRNA in CTCL, and we used qRT-PCR, RNA immunoprecipitation, dual-luciferase assay, RNA pull down and Western Blotting to further detect the relation of miRNA and mRNA. Also, we have verified above results in mice and clinical samples.</div></div><div><h3>Results</h3><div>LncRNA-RN7SL1 was overexpressed in CTCL compared with benign inflammatory dermatosis and was related to the TNMB stage of mycosis fungoides and Sézary syndrome (higher expression in IIB-IVB stage than IA-IIA stage). Additionally, the proliferation of CTCL cell lines HH and Hut78 was weakened, but apoptosis was facilitated by RN7SL1 downregulation, resulting in a reduced tumorigenic capacity in vivo. Subsequently, Whole transcriptome sequencing and target validation indicated that the RN7SL1/miR-34a-5p/MYCN axis may promoted malignant behavior in CTCL.</div></div><div><h3>Conclusion</h3><div>Our study suggested that RN7SL1 promoted malignant behavior by targeting miR-34a-5p/MYCN signaling. This finding might facilitate the discovery of novel biomarkers for CTCL diagnosis and treatment.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"118 1","pages":"Pages 18-28"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744659","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}

引用次数: 0

A signal peptide variant in SLURP1 with dominant-negative effect causes progressive symmetric erythrokeratodermia SLURP1的信号肽变异具有显性阴性作用，可导致进行性对称红角化皮病。

IF 4.6

Journal of dermatological science

Pub Date : 2025-04-01 DOI: 10.1016/j.jdermsci.2025.02.006

Zhuoqing Gong , Yunran Peng , Sisi Zhao , Zhimiao Lin , Zhanli Tang , Huijun Wang

Background

Progressive symmetric erythrokeratodermia (PSEK) is a group of hereditary cornification disorders characterized by symmetrical, progressive erythroderma and hyperkeratosis over the body. Loss-of-function variants in SLURP1, encoding secreted Ly-6/uPAR-related protein 1, is known to cause Mal de Meleda, an autosomal recessive palmoplantar keratoderma.

Objective

To identify the genetic basis and the pathogenesis of a sporadic patient with PSEK.

Methods

Whole-exome sequencing and Sanger sequencing were performed to identify the pathogenic variant(s). The expression of SLURP1 was assessed on the patient’s skin tissue by immunofluorescence. Western blotting (WB) and immunofluorescence (IF) were performed on eukaryotic overexpression systems to evaluate the signal peptide (SP) cleavage, subcellular localization and secretion of the mutant SLURP1. Combined WB and IF analyses were conducted on cells co-transfected with FLAG-tagged wild-type SLURP1 and untagged SLURP1-Ala22Asp.

Results

We identified a de novo heterozygous variant in SLURP1 (c.65A > C, p.Ala22Asp) affecting the first residue before SP cleavage site in a patient with PSEK. This variant abolished the cleavage site of SP, resulting in translocation deficiency to the Golgi apparatus and decreased secretion of the mutant SLURP1. We also found that the SLURP1-Ala22Asp exerted a dominant-negative effect by impeding the SP cleavage of the wild-type SLURP1 and affecting its subcellular localization and secretion in a dose-dependent manner.

Conclusion

We reported the first autosomal-dominant variant in SLURP1 associated with a new phenotype of PSEK in a patient, emphasizing the genetic and clinical heterogeneity of SLURP1-associated genodermatoses.

背景：进行性对称红皮病（PSEK）是一组遗传性角化疾病，其特征是全身对称、进行性红皮病和角化过度。SLURP1编码分泌的Ly-6/ upar相关蛋白1，已知其功能缺失变异可导致掌足底角化病（Mal de Meleda）。目的：探讨散发性PSEK患者的遗传基础和发病机制。方法：采用全外显子组测序和Sanger测序鉴定致病变异。免疫荧光法检测患者皮肤组织中SLURP1的表达。利用Western blotting （WB）和免疫荧光（IF）对真核过表达系统进行检测，评估突变体SLURP1的信号肽（SP）裂解、亚细胞定位和分泌情况。对共转染flag标记的野生型SLURP1和未标记的SLURP1- ala22asp的细胞进行WB和IF联合分析。结果：我们发现了一个新的SLURP1杂合变异（C . 65a > C, p.Ala22Asp），影响PSEK患者SP切割位点前的第一个残基。该变异消除了SP的裂解位点，导致高尔基体易位不足，突变体SLURP1的分泌减少。我们还发现SLURP1- ala22asp通过阻断野生型SLURP1的SP切割，并以剂量依赖的方式影响其亚细胞定位和分泌，从而发挥显性负向作用。结论：我们报道了一例患者中与PSEK新表型相关的SLURP1常染色体显性变异，强调了SLURP1相关的遗传性皮肤病的遗传和临床异质性。

{"title":"A signal peptide variant in SLURP1 with dominant-negative effect causes progressive symmetric erythrokeratodermia","authors":"Zhuoqing Gong , Yunran Peng , Sisi Zhao , Zhimiao Lin , Zhanli Tang , Huijun Wang","doi":"10.1016/j.jdermsci.2025.02.006","DOIUrl":"10.1016/j.jdermsci.2025.02.006","url":null,"abstract":"<div><h3>Background</h3><div>Progressive symmetric erythrokeratodermia (PSEK) is a group of hereditary cornification disorders characterized by symmetrical, progressive erythroderma and hyperkeratosis over the body. Loss-of-function variants in <em>SLURP1</em>, encoding secreted Ly-6/uPAR-related protein 1, is known to cause Mal de Meleda, an autosomal recessive palmoplantar keratoderma.</div></div><div><h3>Objective</h3><div>To identify the genetic basis and the pathogenesis of a sporadic patient with PSEK.</div></div><div><h3>Methods</h3><div>Whole-exome sequencing and Sanger sequencing were performed to identify the pathogenic variant(s). The expression of SLURP1 was assessed on the patient’s skin tissue by immunofluorescence. Western blotting (WB) and immunofluorescence (IF) were performed on eukaryotic overexpression systems to evaluate the signal peptide (SP) cleavage, subcellular localization and secretion of the mutant SLURP1. Combined WB and IF analyses were conducted on cells co-transfected with FLAG-tagged wild-type SLURP1 and untagged SLURP1-Ala22Asp.</div></div><div><h3>Results</h3><div>We identified a <em>de novo</em> heterozygous variant in <em>SLURP1</em> (c.65A > C, p.Ala22Asp) affecting the first residue before SP cleavage site in a patient with PSEK. This variant abolished the cleavage site of SP, resulting in translocation deficiency to the Golgi apparatus and decreased secretion of the mutant SLURP1. We also found that the SLURP1-Ala22Asp exerted a dominant-negative effect by impeding the SP cleavage of the wild-type SLURP1 and affecting its subcellular localization and secretion in a dose-dependent manner.</div></div><div><h3>Conclusion</h3><div>We reported the first autosomal-dominant variant in <em>SLURP1</em> associated with a new phenotype of PSEK in a patient, emphasizing the genetic and clinical heterogeneity of <em>SLURP1</em>-associated genodermatoses.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"118 1","pages":"Pages 38-44"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143538267","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}

引用次数: 0

Topical sirolimus suppresses skin fibrosis in a bleomycin-induced mouse model of systemic sclerosis 局部西罗莫司抑制博来霉素诱导的系统性硬化症小鼠模型的皮肤纤维化。

IF 4.6

Journal of dermatological science

Pub Date : 2025-04-01 DOI: 10.1016/j.jdermsci.2025.02.002

Akiko Sekiguchi , Mai Ishikawa , Akihiko Uchiyama, Yoko Yokoyama, Sachiko Ogino, Ryoko Torii, Sei-ichiro Motegi

引用次数: 0

Thiotaurine inhibits melanoma progression by enhancing Ca2+ overload-induced cellular apoptosis 硫代牛磺酸通过增强 Ca2+ 超载诱导的细胞凋亡抑制黑色素瘤的发展。

IF 4.6

Journal of dermatological science

Pub Date : 2025-04-01 DOI: 10.1016/j.jdermsci.2025.03.001

Di Wang , Ansheng Xie , Jialiang Luo , Lei Li , Zhiwen Zhang , Weiwei Deng , Bin Yang , Yuan Chang , Yunsheng Liang

Background

Melanoma is the most dangerous type of skin cancer with poor therapy outcomes. Since malignant cells are more susceptible to Ca²⁺ overload than normal cells, activating Ca²⁺ overload-mediated apoptosis may be a promising strategy to inhibit melanoma progression. Hydrogen sulfide (H₂S) donors can regulate Ca²⁺ channels, but their effects on melanoma cells remain unclear.

Objective

To explore the effects of Thiotaurine (TTAU), an H₂S donor, on melanoma cells and its underlying mechanisms.

Methods

We tested the effect of TTAU by culturing melanoma cells in vitro and establishing the xenograft model of mice in vivo. Cell proliferation and apoptosis were assessed using the CCK-8 test and flow cytometry. Molecules involved in apoptosis or Ca²⁺-related signal transduction were analyzed by western blotting. Immunofluorescence was used to measure Ca²⁺ levels, mitochondrial damage, and reactive oxygen species (ROS).

Results

TTAU significantly reduced melanoma cell viability and induced apoptosis both in vitro and in vivo. Mechanistically, TTAU increased intracellular Ca²⁺, upregulated transient receptor potential vanilloid 1(TRPV1), and decreased activating transcription factor 3(ATF3) by nuclear factor of activated T cell cytoplasmic 1(NFATc1). TTAU also caused mitochondrial damage and ROS overproduction, which also promoted apoptosis.

Conclusion

We first elucidate that TTAU inhibits melanoma progression by activating Ca²⁺ influx-NFATc1-ATF3 signaling and aggravating mitochondrial oxidative stress, in which TRPV1 may act as an amplifier for Ca²⁺ influx. Our research is expected to provide new ideas for the treatment of tumors such as melanoma, as well as the clinical application of reactive sulfur species-based drugs.

背景：黑色素瘤是最危险的皮肤癌类型，治疗效果差。由于恶性细胞比正常细胞更容易受到Ca2+超载的影响，激活Ca2+超载介导的细胞凋亡可能是抑制黑色素瘤进展的一种有希望的策略。硫化氢（H2S）供体可以调节Ca2+通道，但其对黑色素瘤细胞的影响尚不清楚。目的：探讨硫化氢供体硫牛磺酸（Thiotaurine， TTAU）对黑色素瘤细胞的作用及其机制。方法：通过体外培养黑色素瘤细胞和建立小鼠体内异种移植瘤模型，验证TTAU的作用。采用CCK-8检测和流式细胞术检测细胞增殖和凋亡情况。western blotting分析参与细胞凋亡或Ca2+相关信号转导的分子。免疫荧光用于测量Ca2+水平，线粒体损伤和活性氧（ROS）。结果：TTAU在体外和体内均能显著降低黑色素瘤细胞活力，诱导细胞凋亡。在机制上，TTAU增加了细胞内Ca2+，上调了瞬时受体电位香兰素1(TRPV1)，并通过活化T细胞质1的核因子（NFATc1）降低了活化转录因子3（ATF3）。TTAU还引起线粒体损伤和ROS过量产生，从而促进细胞凋亡。结论：我们首先阐明了TTAU通过激活Ca2+流入- nfatc1 - atf3信号和加重线粒体氧化应激来抑制黑色素瘤的进展，其中TRPV1可能作为Ca2+流入的放大器。我们的研究有望为黑色素瘤等肿瘤的治疗以及活性硫类药物的临床应用提供新的思路。

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引用次数: 0

Triclosan exacerbates atopic dermatitis in mouse models via thymic stromal lymphopoietin 三氯生通过胸腺基质淋巴生成素加重小鼠模型中的特应性皮炎。

IF 4.6

Journal of dermatological science

Pub Date : 2025-04-01 DOI: 10.1016/j.jdermsci.2025.02.007

Marie Charlotte Schuppe , Patryk Porebski , Katharina Klara Hahn , Kexin Liao , Anja Uhmann , Andrea Braun , Prasad Dasari , Michael Peter Schön , Timo Buhl

Background

Triclosan, a common antimicrobial agent, is widely used in personal-care products and as a topical antiseptic in atopic dermatitis (AD).

Objective

This study aimed to evaluate the topical and systemic effect of triclosan on AD in murine models, with a specific focus on the role of thymic stromal lymphopoietin (TSLP).

Methods

AD-like skin disease was induced by topical application of MC903 and house dust mites in female wildtype BALB/c, C57BL/6 J, and TSLP receptor (TSLPR)-knockout mouse strains. Mice were treated with triclosan both topically and systemically. Skin inflammation was assessed by measuring ear thickness. Infiltration of immune cells was analyzed by flow cytometry and immunohistochemistry (IHC). Cytokine expression was determined by quantitative real-time PCR.

Results

Triclosan application induced skin inflammation in a dose-dependent manner. Topical triclosan treatment increased ear inflammation and immune cell infiltration in AD-like mouse models. Systemic administration of triclosan also enhanced local AD-like skin reactions. Triclosan-induced skin inflammation was reduced in TSLP-receptor-knockout mice or by blocking TSLP, thus indicating the pivotal role of TSLP in mediating the immunological effects of triclosan.

Conclusions

Topical and systemic administration of triclosan exacerbates AD-like skin inflammation in murine models, with TSLP being a central mediator of this process. The translational relevance of these findings to human disease remains uncertain, as no direct human data are available.

背景：三氯生是一种常见的抗菌药物，广泛应用于个人护理产品和特应性皮炎（AD）的局部抗菌剂。目的：本研究旨在评估三氯生对小鼠AD模型的局部和全身作用，特别关注胸腺基质淋巴生成素（TSLP）的作用。方法：对BALB/c、C57BL/6 J和TSLP受体（TSLPR）敲除的雌性野生型小鼠，局部应用MC903和室内尘螨诱导ad样皮肤病。小鼠局部和全身给予三氯生治疗。通过测量耳部厚度来评估皮肤炎症。采用流式细胞术和免疫组织化学（IHC）分析免疫细胞浸润情况。实时荧光定量PCR检测细胞因子表达。结果：应用三氯生诱导皮肤炎症呈剂量依赖性。局部三氯生治疗增加ad样小鼠模型的耳部炎症和免疫细胞浸润。全身给药三氯生也增强了局部ad样皮肤反应。TSLP受体敲除小鼠或通过阻断TSLP可减轻三氯生诱导的皮肤炎症，从而提示TSLP在介导三氯生免疫作用中的关键作用。结论：局部和全身给药三氯生加剧了小鼠模型ad样皮肤炎症，TSLP是这一过程的中心介质。这些发现与人类疾病的转化相关性仍然不确定，因为没有直接的人类数据。

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引用次数: 0

Rapid thawing enhances tissue destruction in a mouse model of cutaneous cryoablation: Insights into oxidative stress and neutrophil activation 快速解冻增强皮肤冷冻消融小鼠模型中的组织破坏：氧化应激和中性粒细胞激活的见解。

IF 4.6

Journal of dermatological science

Pub Date : 2025-04-01 DOI: 10.1016/j.jdermsci.2025.02.003

Akiko Sekiguchi , Mai Ishikawa , Akihiko Uchiyama , Yoko Yokoyama , Sachiko Ogino , Ryoko Torii , Ryoko Akai , Takao Iwawaki , Sei-ichiro Motegi

Background

Cryoablation is an integral therapeutic approach in dermatology for eliminating viral warts and benign tumors by damaging tissue through freeze-thaw cycles. Rapid thawing of the frozen area by warming it with fingertips during cryoablation is a common technique in Japan; however, its efficacy has not been elucidated.

Objective

This study aimed to evaluate the effect of rapid thawing on cryoablation-treated skin and clarify the underlying mechanisms using cryoablation model mice.

Methods

Cryoablation was performed on the dorsal skin of mice using a liquid nitrogen-soaked cotton swab, followed by rapid thawing by warming with fingertips or natural thawing without treatment. The effects on skin ulcers, immune cell infiltration, and oxidative stress were assessed.

Results

Rapid thawing enlarged cryoablation-induced skin ulcers. The numbers of cryoablation-induced CD3⁺ T cells, neutrophils, neutrophil extracellular traps (NETs), and TUNEL⁺ cells increased with rapid thawing. Visualization of oxidative stress in OKD48 transgenic mice showed that oxidative stress signals in the cryoablation-treated area were enhanced with rapid thawing. Real-time PCR analysis of mouse skin demonstrated that cryoblation-induced levels of NOX2 and HO-1 were significantly elevated with rapid thawing. In mouse melanoma tumors treated with cryoablation, rapid thawing significantly inhibited tumor growth and increased the infiltration of neutrophils, NETs, and TUNEL⁺ cells compared to the group without rapid thawing.

Conclusion

Rapid thawing during cryoablation enhances neutrophil and lymphocyte infiltration, increases oxidative stress, and induces cell death, leading to greater tissue destruction in mice. Dermatologists should consider employing rapid thawing techniques during cryoablation when higher therapeutic intensities are required.

背景：冷冻消融术是皮肤科通过冻融循环损伤组织来消除病毒性疣和良性肿瘤的一种整体治疗方法。在日本，在冷冻消融过程中，用指尖加热冷冻区域来快速解冻是一种常见的技术；然而，其功效尚未得到阐明。目的：利用冻融模型小鼠，探讨快速解冻对冻融后皮肤的影响，并阐明其作用机制。方法：用液氮棉签对小鼠背部皮肤进行冷冻消融，然后用指尖加热或不加处理的自然解冻快速解冻。评估了对皮肤溃疡、免疫细胞浸润和氧化应激的影响。结果：冻融引起的皮肤溃疡迅速融化。随着快速解冻，冷冻诱导的CD3+ T细胞、中性粒细胞、中性粒细胞胞外陷阱（NETs）和TUNEL+细胞的数量增加。OKD48转基因小鼠的氧化应激可视化显示，冻融处理区氧化应激信号随着快速解冻而增强。对小鼠皮肤进行实时荧光定量PCR分析发现，快速解冻后，小鼠皮肤中NOX2和HO-1水平显著升高。在冷冻消融处理的小鼠黑色素瘤肿瘤中，与未快速解冻组相比，快速解冻显著抑制肿瘤生长，增加中性粒细胞、NETs和TUNEL+细胞的浸润。结论：冻融过程中快速解冻增加了小鼠中性粒细胞和淋巴细胞的浸润，增加了氧化应激，诱导细胞死亡，导致更大的组织破坏。当需要更高的治疗强度时，皮肤科医生应考虑在冷冻消融期间采用快速解冻技术。

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引用次数: 0

Editors Choice 编辑的选择

IF 4.6

Journal of dermatological science

Pub Date : 2025-04-01 DOI: 10.1016/S0923-1811(25)00052-0

引用次数: 0

JSID’s Fellowship Shiseido Research Grant JSID奖学金资生堂研究基金

IF 4.6

Journal of dermatological science

Pub Date : 2025-04-01 DOI: 10.1016/S0923-1811(25)00054-4

引用次数: 0

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