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

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.

• Authors: Si-Yu Sun, Yu-Mei Cao, Yan-Jie Huo, Fei Qiu, Wen-Juan Quan, Chao-Ping He, Yu Chen, Duan-Fang Liao, Qin-Hui Tuo
• Journal: Cell adhesion & migration (Cell Adh Migr) Vol. 15 Issue 1 Pg. 116-125 (12 2021) ISSN: 1933-6926 [Electronic] United States
• PMID: 33843453 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Co-Repressor Proteins
• DAXX protein, human
• Molecular Chaperones
• curcumin nicotinate
• Niacin
• Proto-Oncogene Proteins c-akt
• PTEN Phosphohydrolase
• Curcumin

Topics

• Atherosclerosis (prevention & control)
• Cell Movement (drug effects)
• Cell Proliferation (drug effects)
• Cells, Cultured
• Co-Repressor Proteins (metabolism)
• Curcumin (analogs & derivatives, chemistry, pharmacology)
• Humans
• Molecular Chaperones (metabolism)
• Muscle, Smooth, Vascular (drug effects, metabolism, pathology)
• Myocytes, Smooth Muscle (drug effects, metabolism, pathology)
• Niacin (analogs & derivatives, chemistry, pharmacology)
• PTEN Phosphohydrolase (metabolism)
• Phenotype
• Proto-Oncogene Proteins c-akt (metabolism)
• Signal Transduction (drug effects)
• Up-Regulation