Chlamydia trachomatis plasmid-encoded protein Pgp3 inhibits apoptosis via the PI3K-AKT-mediated MDM2-p53 axis
Chlamydia trachomatis plasmid-encoded protein Pgp3 inhibits apoptosis via the PI3K-AKT-mediated MDM2-p53 axis
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DOI：
10.1007/s11010-018-3422-9
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发表时间：
2018-08
影响因子：
4.3
通讯作者：
Y. Zou;Wenbo Lei;Sheng-mei Su;Jichang Bu;Shunxing Zhu;Qiulin Huang;Zhongyu Li
中科院分区：
文献类型：
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作者：
Y. Zou;Wenbo Lei;Sheng-mei Su;Jichang Bu;Shunxing Zhu;Qiulin Huang;Zhongyu Li
Chlamydia trachomatis, the most common human pathogen that causes trachoma and sexually transmitted disease, has developed various strategies for inhibiting host cell apoptosis. Activation of the PI3K (phosphoinositide 3-kinase)/AKT-mediated MDM2 (murine double minute 2)-p53 pathway plays a prominent role in the apoptosis resistance arising fromC. trachomatisinfection. However, the precise upstream mechanisms by whichC. trachomatisactivates this pathway have not been adequately investigated. Here, we reveal that the secretedC. trachomatisplasmid-encoded protein Pgp3 inhibits apoptosis in HeLa cells. This process requires the activation of the PI3K/AKT signaling pathway, thereby leading to phosphorylation and nuclear entry of MDM2, and p53 degradation. PI3 K inhibitor LY294002 and MDM2 inhibitor Nutlin-3a block Pgp3-induced inhibition of HeLa cell apoptosis, suggesting a critical role for the PI3K/AKT pathway and its effect on the MDM2-p53 axis in Pgp3 anti-apoptotic activity.
