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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。
Objective To investigate the effect of CPI-17 (PKC-potentiated protein phosphatase inhibitory protein-17) on the formation of atherosclerosis by inducing vascular smooth muscle cell phenotype changes. Methods ApoE-knockout mice were induced to form atherosclerotic plaque by carotid artery cannulation. The wild type C57BL / 6 mice were used as control. The carotid artery was isolated and the total RNA was extracted. Fluorescent quantitative PCR was used to detect the expression of contractile-related proteins-sm-MHC, α-actin in CPI-17 and vascular smooth muscle cells in carotid artery of plaque tissue and control mice. MRNA level. Then, the cells were cultured in ox-LDL (50mg / L ox-LDL) and cultured in hypoxic environment, respectively. The changes of CPI-17 expression were detected by real-time fluorescence quantitative PCR . Results CPI-17 mRNA level and sm-MHC, α-actin in ApoE-knockout mice atherosclerotic plaque cells were significantly lower than those in C57BL / 6 mice, ox-LDL stimulated and hypoxia-cultured MOVAS cells The levels were significantly lower (P <0.05). Conclusion Ox-LDL stimulation and hypoxia culture can decrease the expression of CPI-17 in MOVAS cells, which may be involved in the development of atherosclerosis by regulating the contractile properties of vascular smooth muscle cells.