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J.Health Sci., 57(1), 86-92, 2011
-Research Letter-
Potent Inhibition of Platelet-Derived Growth Factor-Stimulated Rat Aortic Vascular Smooth Muscle Cell Cycle and Proliferation by (2E)-3-(4-hydroxy-3-methoxyphenyl)phenylpro-2-en-1-one, a Newly Synthesized Benzylideneacetophenone Derivative
Tack-Joong Kim,*, a, # Hyeong-Jun Han,b, #
Jae-Chul Jung,c Seikwan Oh,c
and Yeo-Pyo Yund
aDivision of Biological Science and Technology, College of Science and Technology, Yonsei University, Wonju 220-710, Republic of Korea,
bDepartment of Pharmacy, College of Pharmacy, Seoul National University, Seoul 151-742, Republic of Korea,
cDepartment of Neuroscience and Medical Research Institute, School of Medicine, Ewha Womans University, Seoul 158-710, Republic of Korea and
dCollege of Pharmacy, Chungbuk National University, Cheongju 361-763, Republic of Korea
One of the principal regulators of mitogenesis in vascular smooth muscle cells (VSMCs) is platelet-derived growth factor-BB (PDGF-BB). An increase of PDGF-BB expression has been observed in atherosclerotic lesions. The aim of this study was to elucidate the effects and molecular mechanism of (2E)-3-(4-hydroxy-3-methoxyphenyl) phenylpro-2-en-1-one (KTJ2242), a newly synthesized benzylideneacetophenone derivative, on PDGF-BB-stimulated rat aortic VSMCs. KTJ2242 induced accumulation of cells in the G1 phase of the cell cycle of VSMCs. We observed that KTJ2242 inhibited PDGF-BB-stimulated [3H]-thymidine incorporation into the DNA of VSMCs, and the cell number was significantly reduced in a concentration-dependent manner. Also, we observed that KTJ2242 decreased PDGF-BB-stimulated extracellular-regulated kinase 1 and 2 (ERK1/2) and Akt phosphorylation. These results suggest the possibility that KTJ2242 may be a potential agent with which to control vascular disorders and its antiproliferative mechanism may be mediated through partial Akt and ERK1/2-dependent signaling pathways.
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