Bisdemethoxycurcumin inhibits PDGF-induced vascular smooth muscle cell motility and proliferation
Version of Record online: 2 APR 2013
© 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
Molecular Nutrition & Food Research
Special Issue: Curcumin: Recent Insights, Novel Developments, New Challenges
Volume 57, Issue 9, pages 1611–1618, September 2013
How to Cite
Hua, Y., Dolence, J., Ramanan, S., Ren, J. and Nair, S. (2013), Bisdemethoxycurcumin inhibits PDGF-induced vascular smooth muscle cell motility and proliferation. Mol. Nutr. Food Res., 57: 1611–1618. doi: 10.1002/mnfr.201200852
- Issue online: 2 SEP 2013
- Version of Record online: 2 APR 2013
- Manuscript Accepted: 19 JAN 2013
- Manuscript Received: 21 DEC 2012
- Manuscript Revised: 21 DEC 2012
- National Center for Research Resources. Grant Number: 5P20RR016474-12
- National Institute of General Medical Sciences. Grant Number: 8 P20 GM103432-12
- National Institutes of Health
- Platelet-derived growth factor;
- Vascular smooth muscle cell
A key event in the development of plaque in the arteries is the migration and proliferation of smooth muscle cells (SMCs) 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 SMCs.
Methods and results
CC and BC were synthesized by condensing acetyl acetone with vanillin and 4-hydroxybenzaldehyde, respectively. SMCs 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 [3H]-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 SMCs. Both compounds were equipotent in inhibiting PDGF-stimulated generation of intracellular reactive oxygen species.
BC may be of potential use in the prevention or treatment of vascular disease.