Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 유충규 | - |
dc.date.accessioned | 2017-01-05T02:01:58Z | - |
dc.date.available | 2017-01-05T02:01:58Z | - |
dc.date.issued | 2008 | - |
dc.identifier.issn | 0006-2952 | - |
dc.identifier.other | OAK-4719 | - |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/233541 | - |
dc.description.abstract | The increased potential for growth of vascular smooth muscle cells (VSMCs) is a key abnormality in the development of atherosclerosis and postangioplasty restenosis. Platelet-derived growth factor (PDGF)-BB is a potent mitogen for VSMCs that plays an important role in the intimal accumulation of VSMCs. This study examined the effect of JM91, a newly synthesized indoledione derivative, on the proliferation of PDGF-BB-stimulated rat aortic VSMCs. The antiproliferative effect of JM91 on rat aortic VSMCs was examined by cell counting and [ 3H]thymidine incorporation assay. The pre-incubation of JM91 (0.5-3.0 μM) significantly inhibited the proliferation and DNA synthesis of 25 ng/mL PDGF-BB-stimulated rat aortic VSMCs in a concentration-dependent manner. JM91 inhibited the PDGF-BB-stimulated phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt kinase, while had no effect on PLCγ1 and PDGF-Rβ activation. In addition, treatment with JM91 (0.5-3.0 μM) induced cell-cycle arrest in the G 1 phase, which was associated with the down-regulation of cyclins and CDKs. These findings suggest that the inhibitory effects of JM91 against proliferation, DNA synthesis and cell cycle progression of PDGF-BB-stimulated rat aortic VSMCs are mediated by the suppression of the ERK1/2 and PI3K/Akt signaling pathways. Furthermore, JM91 may be a potential antiproliferative agent for the treatment of atherosclerosis and angioplasty restenosis. © 2007 Elsevier Inc. All rights reserved. | - |
dc.language | English | - |
dc.title | JM91, a newly synthesized indoledione derivative, inhibits rat aortic vascular smooth muscle cells proliferation and cell cycle progression through inhibition of ERK1/2 and Akt activations | - |
dc.type | Article | - |
dc.relation.issue | 6 | - |
dc.relation.volume | 75 | - |
dc.relation.index | SCIE | - |
dc.relation.index | SCOPUS | - |
dc.relation.startpage | 1331 | - |
dc.relation.lastpage | 1340 | - |
dc.relation.journaltitle | Biochemical Pharmacology | - |
dc.identifier.doi | 10.1016/j.bcp.2007.11.013 | - |
dc.identifier.wosid | WOS:000254687800009 | - |
dc.identifier.scopusid | 2-s2.0-39749093224 | - |
dc.author.google | Seo J.-M. | - |
dc.author.google | Jin Y.-R. | - |
dc.author.google | Ryu C.-K. | - |
dc.author.google | Kim T.-J. | - |
dc.author.google | Han X.-H. | - |
dc.author.google | Hong J.-T. | - |
dc.author.google | Yoo H.-S. | - |
dc.author.google | Lee C.-K. | - |
dc.author.google | Yun Y.-P. | - |
dc.contributor.scopusid | 유충규(15846918400) | - |
dc.date.modifydate | 20170901081001 | - |