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Curcumin Regulates VSMC Phenotype Transition via Modulation of N otch and W nt Signaling Pathways
Author(s) -
Chen Jing,
Xu Lin,
Hu Xiaorong,
Zhang Jing,
Xu Changwu,
Li Guoqing,
Jiang Hong
Publication year - 2013
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.21075
Subject(s) - curcumin , downregulation and upregulation , vascular smooth muscle , chemistry , signal transduction , microbiology and biotechnology , phenotype , stimulation , pharmacology , biology , endocrinology , biochemistry , gene , smooth muscle
Preclinical ResearchIn the development of cardiovascular diseases, vascular smooth muscle cells ( VSMCs ) undergo transition from a contractile to a synthetic phenotype. N otch ‐ and W nt ‐dependent signaling pathways play a critical role during this process. Curcumin has potential for clinical use including anti‐inflammatory and antitumor actions. However, the effect of curcumin on VSMC phenotype transition remains unclear. In VSMCs isolated from the thoracic aorta of S prague D awley rats, curcumin (5–20 μM) produced a concentration‐dependent inhibition of serum‐elicited VSMC migration. Furthermore, curcumin, at the dose of 20 μM, partially reversed the repression of VSMC markers induced by serum stimulation, an effect associated with attenuation of J agged‐1 and N otch‐1 levels and downregulation of the downstream gene H ey‐1 . Downregulation of W nt‐4 was also observed after curcumin treatment in the presence of serum, which was followed by inhibition of nuclear β‐catenin translocation and cyclin D 1 expression. These data suggest that curcumin is a potent regulator of VSMC s phenotype transition and may play a critical role in regulating these events after vascular injury.