表皮生长因子受体及PI3K在硫酸锌诱导人呼吸道上皮细胞间粘附分子-1表达过程中的作用

Involvement of EGF receptor and PI3K in ICAM-1 expression in human airway epithelial cells exposed to zinc sulfate

目的探讨硫酸锌对上皮细胞内细胞间粘附分子-1(ICAM-1)表达的影响及其分子生物学机制。方法应用PCR与蛋白质免疫印迹试验检测硫酸锌诱导人呼吸道上皮细胞ICAM-1mRNA与蛋白的表达,以及表皮生长因子受体(EGFR)及PI3K的活化。结果硫酸锌可诱导ICAM-1mRNA与蛋白的过量表达。在同一试验条件下,硫酸锌可诱发EGFR及磷脂酰肌醇3激酶(PI3K)下游激酶Akt的磷酸化或活化。用EGFR抑制剂(PD153035)及PI3K抑制剂(LY294002)预处理上皮细胞,可明显抑制硫酸锌对ICAM-1表达的诱导作用。结论硫酸锌可激活EGFR与PI3K/Akt信号传导通路,进而上调ICAM-1的表达。

Objective To explore the effect of zinc sulfate on the expression of intercellular adhension molecule 1（ICAM-1） and underlying mechanisms.Methods A human bronchial epithelial cell line（BEAS-2B） was treated with zinc sulfate.The expression of ICAM-1 mRNA and protein and activation of epithelial growth factor receptor（EGFR） and PI3K was determined using PCR and immunoblotting.Results Zinc sulfate stimulation induced overexpression of ICAM-1 mRNA and protein.Under the same experimental condition,exposure to zinc sulfate increased phosphorylation of EGFR and Akt,the downstream kinase of PI3K.Pretreatment of BEAS-2B cells with the EGFR inhibitor PD153035 and the PI3K inhibitor LY294002 significantly blocked zinc sulfate-induced ICAM-1 expression.Conclusion Zinc sulfate stimulation could activate the EGFR and the PI3K/Akt signaling pathway,further leading to upregulation of ICAM-1 expression.