CVB3m激活胞外信号调节激酶(ERK)信号途径

Signaling pathway of extracellular signal-regulated kinase (ERK) activated by CVB3m infection

目的 了解细胞外信号调节激酶 1和 2 (ERK1/2 )途径在柯萨奇病毒B3感染中的作用。方法 感染复数MOI =10的CVB3m或PBS感染生长停滞的HeLa细胞 1小时 ,在指定时间收集细胞裂解液后应用免疫印迹分析感染后不同时间ERK1/2的磷酸化以了解Raf/MEK/ERK途径的活化。结果 CVB3m感染引起HeLa细胞ERK1/2的二次激活。第一次激活在感染后 10min即可检出 ,持续至感染后 1h ,随后P -ERK1/2水平降至基础。在感染后 7h再次激活并一直持续激活至感染后 2 4h ,在感染后 12h达到峰值。结论 CVB3m感染二次激活ERK1/2途径 ,即早期短暂激活和晚期的持续激活。

To determine the role of extracellular signal regulated kinase(ERK) signaling pathway in CVB3m infection.After growth arrested by serum starvation,HeLa cells were infected at multiplicity of infection (MOI) of 10 with CVB3m or sham treated with phosphate buffered saline(PBS) for 1 h.Cell lysates were collected for indicated times following CVB3m infection and subjected to SDS PAGE and Western blotting to analyse ERK1/2 activities based on phosphorylated ERK1/2.CVB3m leads to biphasic activation of ERK1/2 in HeLa cells.It was found that the first activation occurred at 10 min and decreased to baseline after 1 h postinfection.The second activation was apparent between 7 h and 24 h postinfection,and the peak arrived at 12h postinfection.The activation was persistent until 24h postinfection.CVB3m infection induces biphasic activation of ERK1/2.Namely,CVB3m triggers early transient and late sustained biphasic activation of ERK1/2.These findings suggest that ERK1/2 pathway should play an important role in CVB3m infection.