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Two novel MBTPS2 missense mutations impairing S2P proteolytic activity lead to IFAP syndrome with new phenotypic anomalies 损害S2P蛋白水解活性的两个新的MBTPS2错义突变导致具有新表型异常的IFAP综合征。
IF 4.6 Pub Date : 2023-12-01 DOI: 10.1016/j.jdermsci.2023.10.004
Natarin Caengprasath , Mathilde Nizon , Ratchathorn Panchaprateep , Benjamin Cogne , Silvestre Cuinat , Hélène Auburt , Nathalie Jonca , Thantrira Porntaveetus , Vorasuk Shotelersuk
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引用次数: 0
Editor's Choice 编辑推荐
IF 4.6 Pub Date : 2023-12-01 DOI: 10.1016/S0923-1811(23)00262-1
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引用次数: 0
Dual effect of tacrolimus on mast cell–mediated allergy and inflammation through Mas-related G protein-coupled receptor X2 他克莫司通过肥大细胞相关G蛋白偶联受体X2对肥大细胞介导的过敏和炎症的双重作用。
IF 4.6 Pub Date : 2023-12-01 DOI: 10.1016/j.jdermsci.2023.10.003
Xueshan Du , Delu Che , Bin Peng , Yi Zheng , Yong Hao , Tao Jia , Xinyue Zhang , Songmei Geng

Background

Topical tacrolimus, although widely used in the treatment of dermatoses, presents with an immediate irritation on initial application resembling a pseudo-allergic reaction. Mas-related G protein-coupled receptor X2 (MRGPRX2) in mast cells (MCs) mediates drug-induced pseudo-allergic reaction and immunoglobulin E (IgE)-independent pruritis in chronic skin diseases. However, the immunosuppression mechanism of tacrolimus on MCs via MRGPRX2 has not been reported.

Objective

To investigate the role of MRGPRX2 and the mechanism of action of tacrolimus on its short-term and long-term applications.

Methods

Wild-type mice, KitW-sh/W-sh mice, and MrgprB2-deficient (MUT) mice were used to study the effect of tacrolimus on in vivo anaphylaxis model. LAD2 cells and MRGPRX2-knockdown LAD2 cells were specifically used to derive the associated mechanism of the tacrolimus effect.

Results

Short-term application of tacrolimus triggers IgE-independent activation of MCs via MRGPRX2/B2 in both in vivo and in vitro experiments. Tacrolimus binds to MRGPRX2, which was verified by fluorescently labeled tacrolimus in cells. On long-term treatment with tacrolimus, the initial allergic reaction fades away corresponding with the downregulation of MRGPRX2, which leads to decreased release of inflammatory cytokines (P < 0.05 to P < 0.001).

Conclusion

Short-term treatment with tacrolimus induces pseudo-allergic reaction via MRGPRX2/B2 in MCs, whereas long-term treatment downregulates expression of MRGPRX2/B2, which may contribute to its potent immunosuppressive effect in the treatment of various skin diseases.

背景:局部他克莫司虽然广泛用于治疗皮肤病,但在初次应用时表现出立即刺激,类似于伪过敏反应。肥大细胞(MCs)中mass相关G蛋白偶联受体X2 (MRGPRX2)介导慢性皮肤病中药物诱导的假性过敏反应和免疫球蛋白E (IgE)非依赖性瘙痒。然而,他克莫司通过MRGPRX2对MCs的免疫抑制机制尚未见报道。目的:探讨MRGPRX2的作用及他克莫司对其短期和长期应用的作用机制。方法:采用野生型小鼠、KitW-sh/W-sh小鼠和mrgprb2缺陷(MUT)小鼠,研究他克莫司对体内过敏反应模型的影响。LAD2细胞和mrgprx2敲低的LAD2细胞被专门用来推导他克莫司效应的相关机制。结果:在体内和体外实验中,短期应用他克莫司可通过MRGPRX2/B2触发MCs的ige非依赖性激活。他克莫司与MRGPRX2结合,通过荧光标记他克莫司在细胞中进行验证。长期服用他克莫司,初始过敏反应逐渐消失,MRGPRX2下调,导致炎症细胞因子释放减少(P)结论:短期服用他克莫司可通过MRGPRX2/B2诱导MCs假过敏反应,而长期服用他克莫司可下调MRGPRX2/B2的表达,这可能是其治疗多种皮肤病的有效免疫抑制作用的原因之一。
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引用次数: 0
Late inflammatory monocytes define circulatory immune dysregulation observed in skin microbiome-stratified atopic dermatitis 晚期炎性单核细胞确定了皮肤微生物分层特应性皮炎中观察到的循环免疫失调
IF 4.6 Pub Date : 2023-12-01 DOI: 10.1016/j.jdermsci.2023.10.006
Celine Chua , Raman Sethi , Jocelyn Ong , Jing hui Low , Yik W. Yew , Alicia Tay , Shanshan W. Howland , Florent Ginhoux , Jinmiao Chen , John E.A. Common , Anand K. Andiappan
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引用次数: 0
A20 ameliorates advanced glycation end products-induced melanogenesis by inhibiting NLRP3 inflammasome activation in human dermal fibroblasts A20通过抑制人真皮成纤维细胞中NLRP3炎症小体的激活,改善晚期糖基化终产物诱导的黑色素生成。
IF 4.6 Pub Date : 2023-11-01 DOI: 10.1016/j.jdermsci.2023.09.002
Mengyao Wang , Xianyin Huang , Mengting Ouyang , Jingjing Lan, Jingqian Huang, Hongpeng Li, Wei Lai, Yifeng Gao, Qingfang Xu

Background

Advanced glycation end products (AGEs) promote melanogenesis through activating NLRP3 inflammasome in fibroblasts. Although A20 has been highlighted to inhibit NLRP3 inflammasome activation, its roles and mechanisms remain elusive in photoaging-associated pigmentation.

Objectives

To determine the significance of fibroblast A20 in AGEs-induced NLRP3 inflammasome activation and pigmentation.

Methods

The correlation between A20 and AGEs or melanin was studied in sun-exposed skin and lesions of melasma and solar lentigo. We then investigated A20 level in AGEs-treated fibroblast and the effect of fibroblast A20 overexpression or knockdown on AGEs-BSA-induced NLRP3 inflammasome activation and pigmentation, respectively. Finally, the severity of NLRP3 inflammasome activation and pigmentation was evaluated after mice were injected intradermally with A20-overexpression adeno-associated virus and AGEs-BSA.

Results

Dermal A20 expression was decreased and exhibited negative correlation with either dermal AGEs deposition or epidermal melanin level in sun-exposed skin and pigmentary lesions. Moreover, both AGEs-BSA and AGEs-collagen robustly decreased A20 expression via binding to RAGE in fibroblasts. Further, A20 overexpression or depletion significantly decreased or augmented AGEs-BSA-induced activation of NF-κB pathway and NLRP3 inflammasome and IL-18 production and secretion in fibroblasts, respectively. Importantly, fibroblast A20 potently repressed AGEs-BSA-stimulated melanin content,tyrosinase activity,and expression of microphthalmia-associated transcription factor and tyrosinase in melanocytes. Particularly, fibroblast A20 significantly abrogated AGEs-BSA-promoted melanogenesis in ex vivo skin and mouse models. Additionally, fibroblast A20 inhibited AGEs-BSA-activated MAPKs in melanocytes and the epidermis of ex vivo skin.

Conclusions

Fibroblast A20 suppresses AGEs-stimulate melanogenesis in photoaging-associated hyperpigmentation disorders by inhibiting NLRP3 inflammasome activation.

背景:晚期糖基化终产物(AGEs)通过激活成纤维细胞中的NLRP3炎症小体促进黑色素生成。尽管A20已被强调可抑制NLRP3炎症小体激活,但其在光老化相关色素沉着中的作用和机制仍然难以捉摸。目的:确定成纤维细胞A20在AGEs诱导的NLRP3炎症小体活化和色素沉着中的意义。方法:对日光照射皮肤及黄褐斑、雀斑病变中A20与AGEs或黑色素的相关性进行研究。然后,我们分别研究了AGEs处理的成纤维细胞中A20水平以及成纤维细胞A20过表达或敲低对AGEs-BSA诱导的NLRP3炎症小体激活和色素沉着的影响。最后,在小鼠皮内注射A20过表达腺相关病毒和AGEs-BSA后,评估NLRP3炎症小体激活和色素沉着的严重程度。结果:皮肤A20表达降低,并与暴露在阳光下的皮肤和色素病变中的真皮AGEs沉积或表皮黑色素水平呈负相关。此外,AGEs BSA和AGEs胶原都通过与成纤维细胞中的RAGE结合而显著降低A20的表达。此外,A20过表达或缺失分别显著降低或增强了成纤维细胞中AGEs-BSA诱导的NF-κB通路和NLRP3炎症小体的激活以及IL-18的产生和分泌。重要的是,成纤维细胞A20有效抑制AGEs-BSA刺激的黑色素含量、酪氨酸酶活性以及黑色素细胞中小眼相关转录因子和酪氨酸酶的表达。特别地,在离体皮肤和小鼠模型中,成纤维细胞A20显著消除AGEs-BSA促进黑色素生成。此外,成纤维细胞A20抑制黑素细胞和离体皮肤表皮中的AGEs-BSA激活的MAPKs。结论:成纤维细胞A20通过抑制NLRP3炎症小体激活,抑制AGEs刺激光老化相关色素沉着障碍中的黑色素生成。
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引用次数: 0
Molecular insights of human skin epidermal and dermal aging 人类皮肤表皮和真皮老化的分子洞察力
IF 4.6 Pub Date : 2023-11-01 DOI: 10.1016/j.jdermsci.2023.08.006
Taihao Quan

Human skin is the most widespread and abundant type of tissue in the human body. With the passage of time, most of our organs, including a substantial part of the skin, tend to undergo a gradual thinning or decrease in size. As we age, there is a gradual and progressive reduction in the thickness of both the epidermis and dermis layers of our skin. This is primarily attributed to the decline of epidermal stem cells and the loss of dermal collagen, which is the most abundant protein in the human body. Age-related alterations of the epidermis and dermis impair skin structure/function and create a tissue microenvironment that promotes age-related skin diseases, such as impaired skin barrier, delayed wound healing, and skin cancer development. This review will examine the current body of literature pertaining to our knowledge of skin epidermal and dermal aging.

皮肤是人体中分布最广、数量最多的组织类型。随着时间的推移,我们的大部分器官,包括相当一部分皮肤,都会逐渐变薄或缩小。随着年龄的增长,皮肤表皮层和真皮层的厚度会逐渐减少。这主要归因于表皮干细胞的减少和真皮胶原蛋白的流失,而胶原蛋白是人体中最丰富的蛋白质。表皮层和真皮层与年龄有关的变化会损害皮肤结构/功能,并形成一种组织微环境,促进与年龄有关的皮肤疾病,如皮肤屏障受损、伤口愈合延迟和皮肤癌的发生。本综述将研究目前有关皮肤表皮和真皮老化知识的文献。
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引用次数: 3
Transient receptor potential vanilloid 4 promotes cutaneous wound healing by regulating keratinocytes and fibroblasts migration and collagen production in fibroblasts in a mouse model 在小鼠模型中,瞬时受体电位香草素4通过调节角质形成细胞和成纤维细胞的迁移以及成纤维细胞中胶原的产生来促进皮肤伤口愈合。
IF 4.6 Pub Date : 2023-11-01 DOI: 10.1016/j.jdermsci.2023.10.002
Bayarmaa Taivanbat , Sahori Yamazaki , Bolor Nasanbat , Akihiko Uchiyama , Syahla Nisaa Amalia , Munkhjargal Nasan-Ochir , Yuta Inoue , Mai Ishikawa , Keiji Kosaka , Akiko Sekiguchi , Sachiko Ogino , Yoko Yokoyama , Ryoko Torii , Mari Hosoi , Koji Shibasaki , Sei-ichiro Motegi

Background

Transient receptor potential vanilloid 4 (TRPV4), a cation ion channel, is expressed in different cells, and it regulates the development of different diseases. We recently found a high TRPV4 expression in the wounded skin area. However, the role of TRPV4 in cutaneous wound healing is unknown.

Objective

To investigate the role of TRPV4 in cutaneous wound healing in a mouse model.

Methods

Skin wound healing experiment and histopathological studies were performed between WT and TRPV4 KO mice. The effect of TRPV4 antagonist and agonist on cell migration, proliferation, and differentiation were examined in vitro.

Results

TRPV4 expression was enhanced in wounded area in the skin. TRPV4 KO mice had impaired cutaneous wound healing compared with the WT mice. Further, they had significantly suppressed re-epithelialization and formation of granulation tissue, amount of collagen deposition, and number of α-SMA-positive myofibroblasts in skin wounds. qPCR revealed that the KO mice had decreased mRNA expression of COL1A1 and ACTA2 in skin wounds. In vitro, treatment with selective TRPV4 antagonist suppressed migrating capacity, scratch stimulation enhanced the expression of phospho-ERK in keratinocytes, and TGF-β stimulation enhanced the mRNA expression of COL1A1 and ACTA2 in fibroblasts. Selective TRPV4 agonist suppressed cell migration in keratinocytes, and did not enhance proliferation and migration, but promoted differentiation in fibroblasts.

Conclusion

TRPV4 mediates keratinocytes and fibroblasts migration and increases collagen deposition in the wound area, thereby promoting cutaneous wound healing.

背景:瞬时受体电位香草素4(TRPV4)是一种阳离子通道,在不同的细胞中表达,它调节不同疾病的发展。我们最近发现TRPV4在受伤的皮肤区域有高表达。然而,TRPV4在皮肤伤口愈合中的作用尚不清楚。目的:探讨TRPV4在小鼠皮肤创伤愈合中的作用。方法:在WT和TRPV4 KO小鼠之间进行皮肤创伤愈合实验和组织病理学研究。体外检测TRPV4拮抗剂和激动剂对细胞迁移、增殖和分化的影响。结果:TRPV4在皮肤损伤区表达增强。与WT小鼠相比,TRPV4 KO小鼠的皮肤伤口愈合受损。此外,它们显著抑制了皮肤伤口中上皮再上皮化和肉芽组织的形成、胶原沉积量和α-SMA阳性肌成纤维细胞的数量。qPCR显示KO小鼠在皮肤伤口中COL1A1和ACTA2的mRNA表达降低。在体外,用选择性TRPV4拮抗剂处理抑制了迁移能力,划痕刺激增强了角质形成细胞中磷酸ERK的表达,TGF-β刺激增强了成纤维细胞中COL1A1和ACTA2的mRNA表达。选择性TRPV4激动剂抑制角质形成细胞的细胞迁移,不增强增殖和迁移,但促进成纤维细胞的分化。结论:TRPV4介导角质形成细胞和成纤维细胞迁移,增加伤口胶原沉积,从而促进皮肤伤口愈合。
{"title":"Transient receptor potential vanilloid 4 promotes cutaneous wound healing by regulating keratinocytes and fibroblasts migration and collagen production in fibroblasts in a mouse model","authors":"Bayarmaa Taivanbat ,&nbsp;Sahori Yamazaki ,&nbsp;Bolor Nasanbat ,&nbsp;Akihiko Uchiyama ,&nbsp;Syahla Nisaa Amalia ,&nbsp;Munkhjargal Nasan-Ochir ,&nbsp;Yuta Inoue ,&nbsp;Mai Ishikawa ,&nbsp;Keiji Kosaka ,&nbsp;Akiko Sekiguchi ,&nbsp;Sachiko Ogino ,&nbsp;Yoko Yokoyama ,&nbsp;Ryoko Torii ,&nbsp;Mari Hosoi ,&nbsp;Koji Shibasaki ,&nbsp;Sei-ichiro Motegi","doi":"10.1016/j.jdermsci.2023.10.002","DOIUrl":"10.1016/j.jdermsci.2023.10.002","url":null,"abstract":"<div><h3>Background</h3><p>Transient receptor potential vanilloid 4 (TRPV4), a cation ion channel, is expressed in different cells, and it regulates the development of different diseases. We recently found a high TRPV4 expression in the wounded skin area. However, the role of TRPV4 in cutaneous wound healing is unknown.</p></div><div><h3>Objective</h3><p>To investigate the role of TRPV4 in cutaneous wound healing in a mouse model.</p></div><div><h3>Methods</h3><p>Skin wound healing experiment and histopathological studies were performed between WT and TRPV4 KO mice. The effect of TRPV4 antagonist and agonist on cell migration, proliferation, and differentiation were examined in vitro.</p></div><div><h3>Results</h3><p><span>TRPV4 expression was enhanced in wounded area in the skin. TRPV4 KO mice had impaired cutaneous wound healing compared with the WT mice. Further, they had significantly suppressed re-epithelialization and formation of granulation tissue, amount of collagen deposition, and number of α-SMA-positive myofibroblasts in skin wounds. qPCR revealed that the KO mice had decreased mRNA expression of COL1A1 and ACTA2 in skin wounds. </span><em>In vitro</em><span><span>, treatment with selective TRPV4 antagonist suppressed migrating capacity, scratch stimulation enhanced the expression of phospho-ERK in </span>keratinocytes, and TGF-β stimulation enhanced the mRNA expression of COL1A1 and ACTA2 in fibroblasts. Selective TRPV4 agonist suppressed cell migration in keratinocytes, and did not enhance proliferation and migration, but promoted differentiation in fibroblasts.</span></p></div><div><h3>Conclusion</h3><p>TRPV4 mediates keratinocytes and fibroblasts migration and increases collagen deposition in the wound area, thereby promoting cutaneous wound healing.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"112 2","pages":"Pages 54-62"},"PeriodicalIF":4.6,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41242652","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
Presence of microfibril associated glycoprotein 4 and type V collagen and the possible absence of fibrillin-1 in bead-like structures in elastofibroma 弹性纤维瘤中微纤维相关糖蛋白4和V型胶原的存在以及珠状结构中可能不存在原纤维蛋白-1。
IF 4.6 Pub Date : 2023-11-01 DOI: 10.1016/j.jdermsci.2023.09.005
Haruto Nishida , Takako Sasaki , Yuki Taga , Yusuke Murasawa , Siro Simizu , Shigeto Matsushita , Zenzo Isogai , Shunji Hattori , Tsutomu Daa , Nobuo Nagamine , Akihiro Sekine , Sakuhei Fujiwara
{"title":"Presence of microfibril associated glycoprotein 4 and type V collagen and the possible absence of fibrillin-1 in bead-like structures in elastofibroma","authors":"Haruto Nishida ,&nbsp;Takako Sasaki ,&nbsp;Yuki Taga ,&nbsp;Yusuke Murasawa ,&nbsp;Siro Simizu ,&nbsp;Shigeto Matsushita ,&nbsp;Zenzo Isogai ,&nbsp;Shunji Hattori ,&nbsp;Tsutomu Daa ,&nbsp;Nobuo Nagamine ,&nbsp;Akihiro Sekine ,&nbsp;Sakuhei Fujiwara","doi":"10.1016/j.jdermsci.2023.09.005","DOIUrl":"10.1016/j.jdermsci.2023.09.005","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"112 2","pages":"Pages 112-116"},"PeriodicalIF":4.6,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50164209","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
Painting and dissecting Epidermolysis Bullosa Simplex-associated keratin aggregates 绘制和解剖大疱性表皮松解症相关角蛋白聚集体。
IF 4.6 Pub Date : 2023-11-01 DOI: 10.1016/j.jdermsci.2023.08.007
Katrin Rietscher , Melanie Homberg , Ilya Kovalenko , Jonathan Z. Sexton , Robert H. Rice , Cristina Has , M. Bishr Omary , Thomas M. Magin
{"title":"Painting and dissecting Epidermolysis Bullosa Simplex-associated keratin aggregates","authors":"Katrin Rietscher ,&nbsp;Melanie Homberg ,&nbsp;Ilya Kovalenko ,&nbsp;Jonathan Z. Sexton ,&nbsp;Robert H. Rice ,&nbsp;Cristina Has ,&nbsp;M. Bishr Omary ,&nbsp;Thomas M. Magin","doi":"10.1016/j.jdermsci.2023.08.007","DOIUrl":"10.1016/j.jdermsci.2023.08.007","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"112 2","pages":"Pages 109-111"},"PeriodicalIF":4.6,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41175913","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
In vitro evaluation of Neosetophomone B inducing apoptosis in cutaneous T cell lymphoma by targeting the FOXM1 signaling pathway 靶向FOXM1信号通路诱导皮肤T细胞淋巴瘤细胞凋亡的体外评价。
IF 4.6 Pub Date : 2023-11-01 DOI: 10.1016/j.jdermsci.2023.10.001
Shilpa Kuttikrishnan , Tariq Masoodi , Fareed Ahmad , Gulab Sher , Kirti S. Prabhu , Jericha M. Mateo , Joerg Buddenkotte , Tamam El-Elimat , Nicholas H. Oberlies , Cedric J. Pearce , Ajaz A. Bhat , Feras Q. Alali , Martin Steinhoff , Shahab Uddin

Background

Cutaneous T cell lymphoma (CTCL) is a T cell-derived non-Hodgkin lymphoma primarily affecting the skin, with treatment posing a significant challenge and low survival rates.

Objective

In this study, we investigated the anti-cancer potential of Neosetophomone B (NSP-B), a fungal-derived secondary metabolite, on CTCL cell lines H9 and HH.

Methods

Cell viability was measured using Cell counting Kit-8 (CCK8) assays. Apoptosis was measured by annexin V/PI dual staining. Immunoblotting was performed to examine the expression of proteins. Applied Biosystems' high-resolution Human Transcriptome Array 2.0 was used to examine gene expression.

Results

NSP-B induced apoptosis in CTCL cells by activating mitochondrial signaling pathways and caspases. We observed downregulated expression of BUB1B, Aurora Kinases A and B, cyclin-dependent kinases (CDKs) 4 and 6, and polo-like kinase 1 (PLK1) in NSP-B treated cells, which was further corroborated by Western blot analysis. Notably, higher expression levels of these genes showed reduced overall and progression-free survival in the CTCL patient cohort. FOXM1 and BUB1B expression exhibited a dose-dependent reduction in NSP-B-treated CTCL cells.FOXM1 silencing decreased cell viability and increased apoptosis via BUB1B downregulation. Moreover, NSP-B suppressed FOXM1-regulated genes, such as Aurora Kinases A and B, CDKs 4 and 6, and PLK1. The combined treatment of Bortezomib and NSP-B showed greater efficacy in reducing CTCL cell viability and promoting apoptosis compared to either treatment alone.

Conclusion

Our findings suggest that targeting the FOXM1 pathway may provide a promising therapeutic strategy for CTCL management, with NSP-B offering significant potential as a novel treatment option.

背景:皮肤T细胞淋巴瘤(CTCL)是一种主要影响皮肤的T细胞衍生的非霍奇金淋巴瘤,其治疗具有重大挑战性和低生存率。目的:在本研究中,我们研究了真菌衍生的次级代谢产物新毛霉素B(NSP-B)对CTCL细胞系H9和HH的抗癌潜力。方法:使用细胞计数Kit-8(CCK8)测定细胞活力。膜联蛋白V/PI双染色法检测细胞凋亡。进行免疫印迹以检测蛋白质的表达。应用生物系统公司的高分辨率人类转录组阵列2.0用于检测基因表达。结果:NSP-B通过激活线粒体信号通路和胱天蛋白酶诱导CTCL细胞凋亡。我们观察到,在NSP-B处理的细胞中,BUB1B、Aurora激酶A和B、细胞周期蛋白依赖性激酶(CDKs)4和6以及polo-like激酶1(PLK1)的表达下调,Western印迹分析进一步证实了这一点。值得注意的是,在CTCL患者队列中,这些基因的高表达水平显示出总体生存率和无进展生存率降低。FOXM1和BUB1B的表达在NSP-B处理的CTCL细胞中表现出剂量依赖性降低。FOXM1沉默通过BUB1B下调降低细胞活力并增加细胞凋亡。此外,NSP-B抑制FOXM1调节的基因,如极光激酶A和B、CDKs 4和6以及PLK1。与单独治疗相比,硼替佐米和NSP-B的联合治疗在降低CTCL细胞活力和促进细胞凋亡方面显示出更大的疗效。结论:我们的研究结果表明,靶向FOXM1通路可能为CTCL管理提供一种有前景的治疗策略,NSP-B作为一种新的治疗选择具有重要的潜力。
{"title":"In vitro evaluation of Neosetophomone B inducing apoptosis in cutaneous T cell lymphoma by targeting the FOXM1 signaling pathway","authors":"Shilpa Kuttikrishnan ,&nbsp;Tariq Masoodi ,&nbsp;Fareed Ahmad ,&nbsp;Gulab Sher ,&nbsp;Kirti S. Prabhu ,&nbsp;Jericha M. Mateo ,&nbsp;Joerg Buddenkotte ,&nbsp;Tamam El-Elimat ,&nbsp;Nicholas H. Oberlies ,&nbsp;Cedric J. Pearce ,&nbsp;Ajaz A. Bhat ,&nbsp;Feras Q. Alali ,&nbsp;Martin Steinhoff ,&nbsp;Shahab Uddin","doi":"10.1016/j.jdermsci.2023.10.001","DOIUrl":"10.1016/j.jdermsci.2023.10.001","url":null,"abstract":"<div><h3>Background</h3><p>Cutaneous T cell lymphoma<span> (CTCL) is a T cell-derived non-Hodgkin lymphoma primarily affecting the skin, with treatment posing a significant challenge and low survival rates.</span></p></div><div><h3>Objective</h3><p>In this study, we investigated the anti-cancer potential of Neosetophomone B (NSP-B), a fungal-derived secondary metabolite, on CTCL cell lines H9 and HH.</p></div><div><h3>Methods</h3><p><span><span>Cell viability was measured using Cell counting Kit-8 (CCK8) assays. </span>Apoptosis<span> was measured by annexin V/PI dual staining. Immunoblotting was performed to examine the expression of proteins. Applied Biosystems' high-resolution Human </span></span>Transcriptome Array 2.0 was used to examine gene expression.</p></div><div><h3>Results</h3><p><span><span>NSP-B induced apoptosis in CTCL cells by activating mitochondrial signaling pathways and </span>caspases<span>. We observed downregulated expression of BUB1B, Aurora Kinases A and B, cyclin-dependent kinases (CDKs) 4 and 6, and polo-like kinase 1 (PLK1) in NSP-B treated cells, which was further corroborated by Western blot analysis. Notably, higher expression levels of these genes showed reduced overall and progression-free survival in the CTCL patient cohort. FOXM1 and BUB1B expression exhibited a dose-dependent reduction in NSP-B-treated CTCL cells.FOXM1 silencing decreased cell viability and increased apoptosis via BUB1B downregulation. Moreover, NSP-B suppressed FOXM1-regulated genes, such as Aurora Kinases A and B, CDKs 4 and 6, and PLK1. The combined treatment of </span></span>Bortezomib and NSP-B showed greater efficacy in reducing CTCL cell viability and promoting apoptosis compared to either treatment alone.</p></div><div><h3>Conclusion</h3><p>Our findings suggest that targeting the FOXM1 pathway may provide a promising therapeutic strategy for CTCL management, with NSP-B offering significant potential as a novel treatment option.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"112 2","pages":"Pages 83-91"},"PeriodicalIF":4.6,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49686677","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
期刊
Journal of dermatological science
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