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Bisdemethoxycurcumin inhibits PDGF ‐induced vascular smooth muscle cell motility and proliferation
Author(s) -
Hua Yinan,
Dolence Julia,
Ramanan Shalini,
Ren Jun,
Nair Sreejayan
Publication year - 2013
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201200852
Subject(s) - platelet derived growth factor receptor , protein kinase b , cell growth , microbiology and biotechnology , platelet derived growth factor , chemistry , cell migration , vascular smooth muscle , intracellular , mapk/erk pathway , phosphorylation , growth factor , biology , receptor , biochemistry , cell , endocrinology , smooth muscle
Scope A key event in the development of plaque in the arteries is the migration and proliferation of smooth muscle cells ( SMC s) from the media to the intima of the blood vessel. This study was conducted to evaluate the effects of bisdemethoxycurcumin ( BC ), a naturally occurring structural analog of curcumin ( CC ), on platelet‐derived growth factor ( PDGF )‐stimulated migration and proliferation of SMC s. Methods and results CC and BC were synthesized by condensing acetyl acetone with vanillin and 4‐hydroxybenzaldehyde, respectively. SMC s isolated from adult rat aorta were stimulated with PDGF in the presence or absence of CC or BC following which, cell migration and proliferation were assessed by monolayer wound healing assay and [ 3 H]‐thymidine incorporation respectively. PDGF ‐stimulated phosphorylation of PDGF receptor‐β and its downstream effectors Akt and ERK were assessed by Western blotting. Intracellular reactive oxygen species was assessed using the fluorescent dye 5‐(6)‐chloromethyl‐2′,7′‐dichlorodihydrofluorescein diacetate. BC elicited a concentration‐dependent inhibition of PDGF ‐stimulated phosphorylation of PDGF receptor‐β, Akt and Erk as well as the PDGF ‐stimulated SMC migration and proliferation. BC was more potent than CC in inhibiting migration and proliferation and suppressing PDGF ‐signaling in SMC s. Both compounds were equipotent in inhibiting PDGF ‐stimulated generation of intracellular reactive oxygen species. Conclusion BC may be of potential use in the prevention or treatment of vascular disease.