肺炎衣原体感染通过PI3K通路诱导血管内皮细胞迁移  

Infection of Chlamydia pneumoniae promotes the migration of vascular endothelial cells via PI3K signaling pathway

作　　者：权伟[1] 张利军[1] 陈宁[1] 沈炳玲[1] 叶静[1] 王蓓蓓[1] 刘欣[1] 张丽莙[1] 

机构地区：[1]天津医科大学基础医学院病理生理学教研室,天津300070

出　　处：《中国病理生理杂志》2010年第7期1290-1294,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.30971225);教育部科学技术研究重点资助项目(No.206008)

摘　　要：目的:研究肺炎衣原体感染对血管内皮细胞迁移的影响及其相关分子机制。方法:创伤修复实验与Transwell实验观察肺炎衣原体感染的血管内皮细胞迁移情况,RT-PCR与ELISA法分别检测PI3K mRNA表达与酶活性。结果:肺炎衣原体感染以时间依赖方式明显促进人内皮细胞素ECV304细胞迁移,且可以显著增强PI3K mRNA表达与酶活性;PI3K特异性抑制剂LY294002可有效抑制肺炎衣原体感染引起的上述变化。结论:肺炎衣原体感染可诱导血管内皮细胞迁移,其机制可能与激活PI3K信号转导通路有关。AIM ： To observe the effect of Chlamydia pneumoniae （ C. pn） infection on the migration of vascular endothelial cells （VEC） and to investigate its possible molecular mechanism. METHODS ： The wound - healing assay and transwell assay were performed to observe the effect of C. pn infection on the VEC migration. The mRNA expression and activity of PI3K were measured by RT- PCR and ELISA. RESULTS： Infection of C. pn promoted VEC migration significantly in a time -dependent manner. The mRNA expression and activity of PI3K were up - regulated. Furthermore, the migration of VEC was suppressed markedly when treated with PI3K inhibitor LY294002, and the mRNA expression and activity of PI3K also decreased correspondingly. CONCLUSION： Infection of C. pn may promote VEC migration via the acti- vation of PI3K signaling pathway.

关 键 词：肺炎衣原体 血管内皮细胞迁移 信号转导 血管新生 磷酸肌醇3-激酶 

分 类 号：R363[医药卫生—病理学]