Illicium verum extract suppresses IFN-γ-induced ICAM-1 expression via blockade of JAK/STAT pathway in HaCaT human keratinocytes

Sung, Yoon‐Young; Kim, Ho Kyoung

doi:10.1016/j.jep.2013.07.013

Cited by 27 publications

(19 citation statements)

References 22 publications

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“…Interestingly, it was reported that inhibition of OSMR results in suppressed IL-31, which was highly expressed in the skin of patients with chronic spontaneous urticaria and was released from isolated basophils accompanied with anti-IgE activation (Raap et al, 2017 ). Moreover, it has been reported that inactivation of the JAK/STAT pathway could help in inhibiting the expression of ICAM-1 induced by IFN-γ in HaCaT human keratinocytes (Sung & Kim, 2013 ). The activated JAK/STAT signaling pathway could stimulate IFNs in order to exert an innate immune response (Cheng et al, 2014 ).…”

Section: Discussionmentioning

confidence: 99%

OSMR gene effect on the pathogenesis of chronic autoimmune Urticaria via the JAK/STAT3 pathway

Luo

Yang

et al. 2018

Mol Med

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BackgroundChronic autoimmune urticaria (CAU) is a common skin disease and remains unclear understanding of pathogenesis in the vast majority of cases. In order to explore a new therapy for CAU, the current study was performed to investigate the possible functioning of the Oncostatin M receptor (OSMR) gene in the autoimmunity of CAU via regulation of the JAK/STAT3 signaling pathway.MethodsCAU skin tissues from 24 CAU patients and normal skin tissues from normal subjects were collected. Hematoxylin-eosin (HE) staining was conducted to count eosinophils, and immunohistochemistry was carried out to detect the positive rate of OSMR expression in two kinds of skin tissues. A total of 72 Kunming (KM) mice were selected, and 60 mice were used for establishing CAU models and later transfected with different plasmids. The expression of inflammatory factors was evaluated by enzyme-linked immunosorbent assays (ELISA). Expressions of janus kinase (JAK), signal transducer and activator of transcription 3 (STAT3), interferon-stimulated gene 15 (ISG15), CT10-regulated kinase (CRK), and interferon regulatory factor 9 (IRF9) were identified using Western blot assay and reverse transcription quantitative polymerase chain reaction (RT-qPCR). Epithelial cell proliferation was assessed by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) assay, and cell cycle distribution and cell apoptosis were assessed using flow cytometry.ResultsThe findings confirm that OSMR protein expression and histamine release rate are highly elevated in human CAU skin tissues, and the expression of the JAK/STAT3 signaling pathway-related genes (OSMR, JAK2, STAT3, ISG15, CRK and IRF9) was up-regulated. OSMR gene silencing in CAU mice significantly decreases the content of inflammatory factors (IL-1, IL-6, IFN-γ, and IgE), the number of eosinophils, and reduces the expression of the JAK/STAT3 signaling pathway related genes, and further enhances cell proliferation, promotes cell cycle entry and inhibits apoptosis of epithelial cells.ConclusionAll aforementioned results indicate that OSMR gene silencing inhibits the activation of the JAK/STAT3 signaling pathway, thereby suppressing the development of CAU.

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Section: Discussionmentioning

confidence: 99%

OSMR gene effect on the pathogenesis of chronic autoimmune Urticaria via the JAK/STAT3 pathway

Luo

Yang

et al. 2018

Mol Med

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“…The most commonly studied cytokines in this context are strongly associated with either innate (IL-1α, IL-6, and TNF-α) or adaptive immune responses (IL-17A). The choice of this specific set of cytokines was made on the basis of information reported by several research groups [ 6 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 ], addressing cytokine stimulation of keratinocytes ( Figure 2 a). For selection of the best proinflammatory mix to create a Ps model, a detailed evaluation of the individual and possible synergistic effect of selected cytokines (IL-1α, IL-17A, IL-22, oncostatin-M [OsM], TNF-α, and IFN-γ) on the expression of Ps-associated genes was made [ 35 , 36 ].…”

Section: In Vitro Modelsmentioning

confidence: 99%

Models in the Research Process of Psoriasis

Bocheńska

Smolińska

Moskot

et al. 2017

IJMS

112

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Psoriasis is an ancient, universal chronic skin disease with a significant geographical variability, with the lowest incidence rate at the equator, increasing towards the poles. Insights into the mechanisms responsible for psoriasis have generated an increasing number of druggable targets and molecular drugs. The development of relevant in vitro and in vivo models of psoriasis is now a priority and an important step towards its cure. In this review, we summarize the current cellular and animal systems suited to the study of psoriasis. We discuss the strengths and limitations of the various models and the lessons learned. We conclude that, so far, there is no one model that can meet all of the research needs. Therefore, the choice model system will depend on the questions being addressed.

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“…30 Because JAK1 and JAK2 are two critical tyrosine kinases that directly phosphorylate STAT1 at Tyr701 and the overexpression of VP3 inhibited the IFN-g-induced Tyr701 phosphorylation of STAT1, we next determined whether VP3 mediates IFN-g signaling through JAKs. The effects of VP3 overexpression on JAK-mediated IRF1 promoter activation were examined using reporter assays.…”

Section: Fmdv Vp3 Targets At Jaks Level To Regulate Ifn-g-triggered Smentioning

confidence: 99%

Foot-and-mouth disease virus structural protein VP3 degrades Janus kinase 1 to inhibit IFN-γ signal transduction pathways

Jin

Yang

et al. 2016

Cell Cycle

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Illicium verum extract suppresses IFN-γ-induced ICAM-1 expression via blockade of JAK/STAT pathway in HaCaT human keratinocytes

Cited by 27 publications

References 22 publications

OSMR gene effect on the pathogenesis of chronic autoimmune Urticaria via the JAK/STAT3 pathway

OSMR gene effect on the pathogenesis of chronic autoimmune Urticaria via the JAK/STAT3 pathway

Models in the Research Process of Psoriasis

Foot-and-mouth disease virus structural protein VP3 degrades Janus kinase 1 to inhibit IFN-γ signal transduction pathways

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