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Genistein inhibits rat aortic smooth muscle cell proliferation through the induction of p27kip1

Title
Genistein inhibits rat aortic smooth muscle cell proliferation through the induction of p27kip1
Authors
Yu J.-Y.Lee J.-J.Lim Y.Kim T.-J.Jin Y.-R.Sheen Y.Y.Yun Y.-P.
Ewha Authors
신윤용
SCOPUS Author ID
신윤용scopus
Issue Date
2008
Journal Title
Journal of Pharmacological Sciences
ISSN
1347-8613JCR Link
Citation
vol. 107, no. 1, pp. 90 - 98
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Diet is one of the most important factors that influence the risks for cardiovascular diseases. Genistein, an isoflavone found in soy, may benefit the cardiovascular system. Here, we investigated the effect of genistein on platelet-derived growth factor (PDGF)-BB-induced proliferation of primary cultured rat aortic smooth muscle cells (RASMCs). Genistein significantly inhibited 25 ng/ml PDGF-BB-induced RASMC proliferation and [3H]- thymidine incorporation into DNA at 10, 20, and 40 μM. In accordance with these findings, genistein blocked the PDGF-BB-inducible progression through G0/G1 to S phase of the cell cycle in synchronized cells. Western blot analysis showed that genistein not only inhibited phosphorylation of retinoblastoma protein (pRb) and expression of cyclin E, cyclin-dependent kinase (CDK) 2, and proliferating cell nuclear antigen (PCNA) protein, but also inhibited downregulation of cyclin-dependent kinase inhibitor (CKI) p27 kip1. However, genistein did not affect p21cip1, CDK4, and cyclin D1 expression or early signal transduction through PDGF beta-receptor, extracellular signal-regulated kinases 1/2 (ERK1/2), Akt, and phospholipase C (PLC) γ1 phosphorylation. These results suggest that genistein inhibits PDGF-BB-induced RASMC proliferation via G0/G1 arrest in association with induction of p27kip1, which may contribute to the beneficial effects of genistein on the cardiovascular system. ©2008 The Japanese Pharmacological Society.
DOI
10.1254/jphs.08001FP
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약학대학 > 약학과 > Journal papers
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