Nicotinate-curcumin inhibits AngII-induced vascular smooth muscle cell phenotype switching by upregulating Daxx expression

Cell Adhesion & Migration

Si-yu Sun¹  Duan-fang Liao¹  Yan-jie Huo¹  Fei Qiu¹  Yu Chen¹  Yu-mei Cao¹  Qin-hui Tuo¹  Wen-juan Quan¹  Chao-ping He¹ 

[1] Hunan University of Chinese Medicine;

关键词: nicotinate-curcumin;    vascular smooth muscle cells;    phenotype switching;    daxx;   

DOI  :  10.1080/19336918.2021.1909899

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown