肺炎衣原体感染通过PI3K激活Rac1诱导血管平滑肌细胞迁移

IM: To detect the role of Rac1 activation in vascular smooth muscle cell (VSMC) migration induced by Chlamydia pneumoniae (C.pn) infection and determine the effect of Phosphoinositide 3-kinase (PI3K) on Rac1 activation during this process. METHODS: The recombinant plasmid encoding the GST-PBD fusion protein was transformed into the competent bacteria to induce the expression of the fusion protein. Then, the fusion protein was purified. GST-pull down assay was performed to evaluate the activity of Rac1 in C.pn-infected VSMCs pretreated with or without PI3K inhibitor LY294002. Wound-healing assay and Transwell assay were performed to observe the changes of C.pn infection-induced VSMCs migration with or without preincubation of Rac1 inhibitor NSC23766. RESULTS: After the purification of the GST-PBD fusion protein, the enough and biologically active fusion protein was obtained. After VSMCs were infected with C.pn for 24 h, the activity of Rac1 increased significantly and higher than that of control group by GST-pull down assay (P < 0.05); Rac1 activation induced by C.pn infection was inhibited after pretreatment with LY294002 (P < 0.05). The migration ability of C.pn infected-VSMC preincubated with NSC23766 was significantly reduced and lower than that of C.pn infection group by cell migration assays (P < 0.05).　CONCLUSION: C.pn infection induces VSMC migration possibly through stimulating Rac1 activity via PI3K activation.