Bortezomib, a proteasome inhibitor, alleviates atopic dermatitis by increasing claudin 1 protein expression

Kim, Yong-Eun; Cho, Nam‐Joon; Cheon, Seonghye; Kim, Kee K.

doi:10.1016/j.bbrc.2017.08.120

Cited by 11 publications

(11 citation statements)

References 25 publications

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“…CLDN1 regulates the pathogenesis, severity and natural course of human AD, and reduced levels of CLDN1 in AD skin have been inversely correlated with expression of Th2 markers and a propensity to infection . It is noteworthy that restoring the expression of CLDN1 alleviates atopic dermatitis . So regulating tight junctions might involve in the mechanism of attenuation of AD.…”

Section: Introductionmentioning

confidence: 99%

Calycosin alleviates allergic contact dermatitis by repairing epithelial tight junctions via down‐regulating HIF‐1α

Jia

Wang

et al. 2018

J Cellular Molecular Medi

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Calycosin, a bioactive component derived from Astragali Radix (AR; Huang Qi), has been shown to have an effect of anti‐allergic dermatitis with unknown mechanism. This study aims to investigate the mechanism of calycosin related to tight junctions (TJs) and HIF‐1α both in FITC‐induced mice allergic contact dermatitis and in IL‐1β stimulated HaCaT keratinocytes. Th2 cytokines (IL‐4, IL‐5 and IL‐13) were detected by ELISA. The epithelial TJ proteins (occludin, CLDN1 and ZO‐1), initiative key cytokines (TSLP and IL‐33) and HIF‐1α were assessed by Western blot, real‐time PCR, immunohistochemistry or immunofluorescence. Herein, we have demonstrated that allergic inflammation and the Th2 cytokines in ACD mice were reduced significantly by calycosin treatment. Meanwhile, calycosin obviously decreased the expression of HIF‐1α and repaired TJs both in vivo and in vitro. In HaCaT keratinocytes, we noted that IL‐1β induced the deterioration of TJs, as well as the increased levels of TSLP and IL‐33, which could be reversed by silencing HIF‐1α. In addition, administration of 2‐methoxyestradiolin (2‐ME), a HIF‐1α inhibitor,significantly repaired the TJs and alleviated the allergic inflammation in vivo. Furthermore, TJs were destroyed by DMOG or by overexpressing HIF‐1α in HaCaT keratinocytes, and simultaneously, calycosin down‐regulated the expression of HIF‐1α and repaired the TJs in this process. These results revealed that calycosin may act as a potential anti‐allergy and barrier‐repair agent via regulating HIF‐1α in AD and suggested that HIF‐1α and TJs might be possible therapy targets for allergic dermatitis.

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Section: Introductionmentioning

confidence: 99%

Calycosin alleviates allergic contact dermatitis by repairing epithelial tight junctions via down‐regulating HIF‐1α

Jia

Wang

et al. 2018

J Cellular Molecular Medi

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“…In a study from 2011, AD patients (n = 5) were found to have markedly lower expression of CLDN1 compared to healthy controls . This finding has been replicated in other studies, showing that CLDN1 expression can be downregulated by IL‐33 via the STAT3 pathway in keratinocytes , via IL‐13 in bronchial epithelial tissue , and interestingly, that CLDN1 expression can be restored both in human keratinocytes and a murine model of AD by application of the proteasome inhibitor bortezomib .…”

Section: From Disease Understanding To Biomarkers Endotypes and Tarmentioning

confidence: 61%

Personalized medicine—concepts, technologies, and applications in inflammatory skin diseases

Litman

2019

APMIS

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“…TJ aberration is detected in AD patients with a reduced expression of claudin-1 [16,17], claudin-8, claudin-23 [17], and ZO-1 [18] and shows evidence of impaired barrier function. Increasing Claudin-1 expression was found to alleviate AD symptoms in an AD mice model [19]. Polymorphism of CLDN1 encoding claudin-1 is also found in AD patients [16].…”

Section: Tjs Abnormalitiesmentioning

confidence: 98%

Advances in Immune Pathways and Pathogenesis of Atopic Dermatitis

Lee

Yuen

2018

Curr Derm Rep

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Purpose of Review Atopic dermatitis (AD) is a common chronic skin inflammatory disorder characterized by recurrent eczema accompanied by an intractable itch that leads to an impaired quality of life. This review aims to summarize the advances in immune pathways and pathogenesis of AD. Recent Findings We review and summarize the current literature characterizing immune pathways and pathogenesis of AD. The complex interplay among skin barrier deficiency, immunological derangement, microbiome dysbiosis especially Staphylococcus aureus predominance, and pruritus contribute to the development, progression, and chronicity of the disease. Summary AD is a complex and multifactorial disease. The skin barrier, dysbiosis of the skin microbiome, immune dysregulation, and severe itch all play a part in the pathogenesis of AD. Based on this progress, better targeted therapies are now emerging.

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Bortezomib, a proteasome inhibitor, alleviates atopic dermatitis by increasing claudin 1 protein expression

Cited by 11 publications

References 25 publications

Calycosin alleviates allergic contact dermatitis by repairing epithelial tight junctions via down‐regulating HIF‐1α

Calycosin alleviates allergic contact dermatitis by repairing epithelial tight junctions via down‐regulating HIF‐1α

Personalized medicine—concepts, technologies, and applications in inflammatory skin diseases

Advances in Immune Pathways and Pathogenesis of Atopic Dermatitis

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