羊瘙痒因子139A感染的小鼠脑组织中AMPK—ULKl自噬调节通路的研究  

To investigate the AMPK-ULK1 signal transduction pathway in the scrapie 139A infected mice braintissues

作　　者：范学宇[1] 王荟[1] 许尹[1] 邵启祥[1] 董小平 田婵 

机构地区：[1]江苏大学基础医学与医学技术学院免疫学系,镇江212013 [2]中国疾病预防控中心病毒病预防控制所

出　　处：《中华实验和临床病毒学杂志》2014年第2期126-128,共3页Chinese Journal of Experimental and Clinical Virology

摘　　要：目的研究感染羊瘙痒因子139A的小鼠脑组织中自噬的活化及其机制。方法采用WesternBlot方法检测感染羊瘙痒因子139A的小鼠终末期脑组织匀浆中的AMPK、ULKl及其磷酸化水平和LC3II的表达，并对其进行定量分析。结果感染139A毒株的小鼠脑组织终末期脑组织中AMPK、ULKl及其磷酸化水平均表达升高。同时发现LC3II水平增加。结论AMPK-ULKl通路在139A感染的小鼠脑组织中活化并且有可能对自噬的激活起到了重要的作用。Objective To investigate the activation of the autophagy and the signal transduction pathway in the scrapie 139A infected mice brain tissues. Methods The Western Blot was used to evaluate the expression level of AMPK, ULK1, p-AMPK, P-ULKI and LC3 II in the normal and scrapie 139A infected mice brain tissues. Results The expression levels of AMPK, ULK1 and their phosphorylated form p-AMPK （Thr172） , p-ULK1 （Ser555） are markedly up-regulated in the brains of the mice infected with scrapie agent 139A. Furthermore, the expression of LC3 II was also found increased in the brains of 139A infected mice, but not in normal mice. Conclusion AMPK-ULK1 pathway activated and contributed to autophagy in 139A infected mice brain.

关 键 词：蛋白激酶类 羊瘙痒症 自吞噬作用 

分 类 号：R373[医药卫生—病原生物学]