PI3K/Akt在肺炎衣原体感染诱导血管平滑肌细胞迁移中的作用

目的研究PI3K/Akt在肺炎衣原体(Chlamydia pneumoniae,C.pn)感染诱导血管平滑肌细胞(vascularsmooth muscle cell,VSMC)迁移中的作用。方法利用透射电镜鉴定C.pn成功感染VSMC;采用PI3K特异性抑制剂LY294002预处理VSMC后,wound-healing实验和Transwell实验分别观察VSMC迁移能力的改变;Western blot实验检测VSMC内Akt的磷酸化水平。结果透射电镜可观察到感染的VSMC内出现典型的C.pn原体;C.pn感染VSMC 24 h后,细胞迁移实验结果显示C.pn感染组VSMC的迁移能力增强且明显高于正常对照组(P<0.05);Western blot结果显示C.pn感染组Akt的磷酸化表达水平明显上调且高于正常对照组(P<0.05);PI3K特异性抑制剂LY294002可有效抑制C.pn感染诱导的VSMC迁移及Akt的磷酸化。结论 C.pn感染通过激活PI3K/Akt促进VSMC迁移。

Role of PI3K/Akt in Chlamydia Pneumoniae Infection-induced Vascular Smooth Muscle Cell Migration

Aim To investigate the role of PI3K/Akt in vascular smooth muscle cell(VSMC) migration induced by Chlamydia pneumoniae(C.pn) infection.Methods The successful infection of rat VSMCs with C.pn was identified by transmission electron microscope;After VSMCs were pretreated with the specific PI3K inhibitor LY294002,wound-healing assay and Transwell assay were performed to observe the changes in the migration ability of VSMCs;The phosphorylation level of Akt was detected by Western blot.Results The typical C.pn elementary bodies were observed in the infected VSMCs under the transmission electron microscope;The migration ability of VSMCs infected with C.pn was enhanced and significantly higher than that of control group at 24 h postinfection in the cell migration assay(P<0.05);Western blot results showed that the phosphorylation level of Akt was up-regulated and also higher than that of control group at 24 h after infection(P<0.05).The effects of C.pn infection on the VSMC migration and the phosphorylation level of Akt in the VSMCs were significantly inhibited by the specific PI3K inhibitor LY294002.Conclusion C.pn infection may promote VSMC migration via activation of PI3K/Akt.