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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

Title
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
Authors
Kim T.-J.Han H.-J.Jung J.-C.Oh S.Yun Y.-P.
Ewha Authors
오세관정재철
SCOPUS Author ID
오세관scopus
Issue Date
2011
Journal Title
Journal of Health Science
ISSN
1344-9702JCR Link
Citation
vol. 57, no. 1, pp. 86 - 92
Indexed
SCOPUS WOS scopus
Abstract
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. © 2011 The Pharmaceutical Society of Japan.
DOI
10.1248/jhs.57.86
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의학전문대학원 > 의학과 > Journal papers
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