Kawasaki disease: ubiquitin-specific protease 5 promotes endothelial inflammation via TNFα-mediated signaling

促炎细胞因子 基因敲除 下调和上调 肿瘤坏死因子α 细胞因子 信号转导 炎症 泛素 免疫学 细胞生物学 生物 癌症研究 生物化学 基因
作者
Chengcheng Huang,Wang Wang,Hongbiao Huang,Jiaqi Jiang,Yueyue Ding,Xuan Li,Jin Ma,Meng Hou,Xiangqiang Pu,Guanghui Qian,Haitao Lv
出处
期刊:Pediatric Research [Springer Nature]
卷期号:93 (7): 1883-1890 被引量:5
标识
DOI:10.1038/s41390-022-02341-z
摘要

BackgroundThis study aimed to explore the functions of ubiquitin-specific protease 5 (USP5) in the endothelial inflammation of Kawasaki disease (KD).MethodsUSP5 expression levels in HCAECs were examined after stimulation with TNFα or KD sera. The inflammatory cytokine expression level and nuclear factor κB (NF-κB) signaling activation proteins were also investigated in HCAECs by using USP5 overexpression/knockdown lentivirus as well as its small molecule inhibitor vialinin A.ResultsUSP5 expression level is upregulated in HCAECs after stimulation with KD sera. Similarly, the USP5 expression level is also increased in a time- and dose-dependent manner upon TNFα stimulation in HCAECs. Moreover, USP5 sustains proinflammatory cytokine production and NF-κB signaling activation, whereas USP5 knockdown causes the proinflammatory cytokine levels to decrease and suppress NF-κB signaling activation. Notably, the USP5 inhibitor vialinin A can suppress the expression of inflammatory genes induced by TNFα and IL-1β in HCAECs.ConclusionsOur study identified USP5 as a positive regulator of TNFα production and its downstream signaling activation during the inflammatory responses in HCAECs, and demonstrated that its inhibitor vialinin A might serve as a candidate drug for KD therapy to prevent the excessive production of proinflammatory cytokines.Impact USP5 is upregulated in human coronary artery endothelial cells (HCAECs) whether incubated with acute KD sera or TNFα in vitro. USP5 promotes proinflammatory cytokine expression by sustaining NF-κB signaling activation in HCAECs. The USP5 inhibitor vialinin A can suppress the expression levels of proinflammatory cytokines in HCAEC, thus providing a novel mechanism and intervention strategy in KD therapy.
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