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目的探讨连环蛋白p120在炎性细胞因子肿瘤坏死因子-α(TNF-α)介导的肺微血管内皮细胞激活中的作用及其机制。方法使用小干扰RNA(siRNA)下调p120在内皮细胞中的表达,考察TNF-α刺激所引起的转录因子NF-κB激活、细胞间黏附因子ICAM-1表达水平,以及中性粒细胞跨内皮迁移能力;使用NF-κB特异性抑制剂明确p120对炎症性肺损伤的调节机制。结果 TNF-α能够降低内皮细胞p120的表达水平;p120下调加重了TNF-α介导的NF-κB激活、ICAM-1表达水平增高以及中性粒细胞跨内皮迁移,而NF-κB抑制剂则阻断了该效应。结论 p120通过抑制NF-κB活化,在TNF-α介导的肺微血管内皮细胞激活及随后的中性粒细胞跨内皮迁移中起重要的保护作用。
Objective To investigate the role and mechanism of c-catenin p120 in pulmonary microvascular endothelial cell activation mediated by tumor necrosis factor-α (TNF-α). Methods The expression of p120 in endothelial cells was down-regulated by small interfering RNA (siRNA). The activation of NF-κB, the expression of intercellular adhesion molecule ICAM-1 induced by TNF-α stimulation and the transmembrane migration of neutrophils Ability; the use of NF-κB-specific inhibitors clear p120 mechanism of regulation of inflammatory lung injury. Results TNF-α could decrease the expression of p120 in endothelial cells. The down-regulation of p120 aggravated the activation of NF-κB induced by TNF-α, the increased expression of ICAM-1 and the trans-endothelial migration of neutrophils. However, NF- Blocked the effect. Conclusion p120 plays an important protective role in TNF-α-mediated pulmonary microvascular endothelial cell activation and subsequent neutrophil trans-endothelial migration by inhibiting NF-κB activation.