One of the principal regulators of mitogene- sis 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 benzylide- neacetophenone derivative, on PDGF-BB-stimulated rat aortic VSMCs. KTJ2242 induced accumula- tion 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 signifi- cantly 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 po- tential agent with which to control vascular disorders and its antiproliferative mechanism may be mediated through partial Akt and ERK1/2-dependent signaling pathways.
|Number of pages||7|
|Journal||Journal of Health Science|
|State||Published - Feb 2011|
- Cardiovascular disease
- Vascular smooth muscle cell