【摘要】 目的研究CPI-17(PKC-potentiated protein phosphatase inhibitory protein-17)通过诱导血管平滑肌细胞表型改变影响动脉粥样硬化形成的作用。方法载脂蛋白E基因敲除(ApoE-knockout)小鼠经颈动脉套管术诱导形成动脉粥样斑块,以野生型C57BL/6小鼠为对照,分离颈动脉并提取总RNA,采用实时荧光定量PCR技术对比检测斑块组织与对照小鼠颈动脉中CPI-17及血管平滑肌细胞收缩功能相关蛋白-平滑肌肌球蛋白重链(sm-MHC)、α-肌动蛋白(α-actin)的mRNA水平。然后分别用50mg/L氧化型低密度脂蛋白(ox-LDL)刺激及乏氧环境下培养作用于小鼠平滑肌细胞系MOVAS细胞,实时荧光定量PCR检测两种刺激条件下CPI-17表达的变化。结果 ApoE-knockout小鼠粥样斑块平滑肌细胞的CPI-17mRNA水平及sm-MHC、α-actin显著低于C57BL/6小鼠,ox-LDL刺激及乏氧培养的MOVAS细胞的CPI-17表达水平显著降低(P均<0.05)。结论 ox-LDL刺激及乏氧培养使MOVAS细胞的CPI-17表达水平降低,可能通过调控血管平滑肌细胞的收缩特性参与动脉粥样硬化的发生。更多还原

【Abstract】 Objective To investigate the role of CPI-17 in atherosclerosis by inducing a phenotype change in vascular smooth muscle cells. Methods We established an atherosclerotic plaque model using ApoE-knockout mice,separated the carotid artery and extracted the total RNA,and detected the level of CPI-17 mRNA in both atherosclerotic plaque and normal arteries of C57BL/6 mice. Smooth muscle α-actin and sm-MHC were also detected. Furthermore,MOVAS cells were separately stimulated using two methods:ox-LDL at 50mg/L and cultured under hypoxia. Expression of CPI-17 was determined in these cells. Results The level of CPI-17 mRNA in atherosclerotic plaque of ApoE-knockout mice was significantly lower than that in C57BL/6 mice. Expression of smooth muscle α-actin and smooth muscle myosin heavy chain(sm-MHC) were down-regulated in atherosclerotic plaque in comparison with normal arteries. The level of CPI-17 mRNA was down-regulated in MOVAS cells stimulated with ox-LDL and cultured under hypoxia. Conclusion CPI-17 may play an important role during atherosclerosis by inducing phenotype change of vascular smooth muscle cells.更多还原