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首页> 外文期刊>Journal of Medical Microbiology: An Official Journal of the Pathological Society of Great Britain and Ireland >Chlamydia pneumoniae infection induces vascular smooth muscle cell migration via Rac1 activation
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Chlamydia pneumoniae infection induces vascular smooth muscle cell migration via Rac1 activation

机译:Chlamydia肺炎感染通过RAC1激活诱导血管平滑肌细胞迁移

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Chlamydia pneumoniae infection has been shown to be associated with the development of atherosclerosis by promoting the migration of vascular smooth muscle cells (VSMCs). However, how C. pneumoniae infection induces VSMC migration is not fully understood. A primary role of Ras-related C3 botulinum toxin substrate 1 (Rac1) is to generate a protrusive force at the leading edge that contributes to cell migration. Whether Rac1 activation plays a role in C. pneumoniae infection-induced VSMC migration is not well defined. In the present study, we therefore examined Rac1 activation in C. pneumoniae-infected rat primary VSMCs and the role of Rac1 activation in C. pneumoniae infection-induced VSMC migration. Glutathione S-transferase pull-down assay results showed that Rac1 was activated in C. pneumoniae-infected rat primary VSMCs. A Rac1 inhibitor, NSC23766 (50 μM,) suppressed Rac1 activation stimulated by C. pneumoniae infection, and thereby inhibited C. pneumoniae infection-induced VSMC migration. In addition, C. pneumoniae infection-induced Rac1 activation in the VSMCs was blocked by LY294002 (25 μM), an inhibitor of phosphatidylinositol 3-kinase (PI3K). Taken together, these data suggest that C. pneumoniae infection promotes VSMC migration, possibly through activating Rac1 via PI3K.
机译:通过促进血管平滑肌细胞(VSMC)的迁移,衣原体肺炎感染已被证明与动脉粥样硬化的发展有关。然而,C.肺炎肺炎感染如何诱导VSMC迁移尚未完全理解。 RAS相关C3肉毒杆菌毒素谱系1(RAC1)的主要作用是在有助于细胞迁移的前缘产生突出力。 RAC1激活是否在C.肺炎感染引起的VSMC迁移中发挥作用,没有明确定义。因此,在本研究中,我们研究了C.肺炎肺炎的RAC1活化的RAC1激活,以及RAC1活化在C.肺炎肺炎感染诱导的VSMC迁移中的作用。谷胱甘肽S转移酶下拉测定结果表明,在C.肺炎肺炎感染大鼠原发性VSMC中被激活RAC1。 RAC1抑制剂,NSC23766(50μm,)抑制C.肺炎感染刺激的RAC1活化,从而抑制肺炎肺炎感染诱导的VSMC迁移。此外,VSMCS中的肺炎肺炎感染诱导的RAC1激活通过LY294002(25μm),磷脂酰肌醇3-激酶(PI3K)的抑制剂阻断。在一起,这些数据表明C.肺炎肺炎感染促进了VSMC迁移,可能通过通过PI3K激活RAC1。

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