ABSTRACT

Phenotypic switching is the main cause of the abnormal proliferation and migration of vascular smooth muscle cells (VSMCs). We previously showed that Daxx exerted negative regulatory effect on AngII-induced VSMC proliferation and migration. However, the function of Daxx in VSMC phenotype switching remained unknown. Nicotinate-curcumin (NC) is an esterification derivative of niacin and curcumin that can prevent the formation of atherosclerosis. We found that NC significantly decreased AngII-induced VSMC phenotype switching. Furthermore, NC significantly inhibited AngII-induced cell proliferation and migration. Moreover, NC upregulated Daxx expression and regulated the PTEN/Akt signaling pathway. We concluded that NC inhibited AngII-induced VSMC phenotype switching by regulating the PTEN/Akt pathway, and through a mechanism that might be associated with the upregulation of Daxx expression.

摘要

表型转换是血管平滑肌细胞（VSMCs）异常增殖和迁移的主要原因。我们之前表明 Daxx 对 AngII 诱导的 VSMC 增殖和迁移发挥负调控作用。然而，Daxx 在 VSMC 表型转换中的功能仍然未知。烟酸-姜黄素（NC）是烟酸和姜黄素的酯化衍生物，可以防止动脉粥样硬化的形成。我们发现 NC 显着降低了 AngII 诱导的 VSMC 表型转换。此外，NC 显着抑制 AngII 诱导的细胞增殖和迁移。此外，NC 上调 Daxx 表达并调节 PTEN/Akt 信号通路。我们得出结论，NC 通过调节 PTEN/Akt 通路抑制 AngII 诱导的 VSMC 表型转换，