Source:http://linkedlifedata.com/resource/pubmed/id/17706465
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2007-10-1
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pubmed:abstractText |
Epothilone D (Epo-D) is a paclitaxel-like microtubule-stabilizing agent that was isolated from the myxobacterium Sorangium cellulosum. Although Epo-D can inhibit proliferation in multiple tumor cell lines, the effect of Epo-D on neointimal hyperplasia after angioplasty has not been reported. The aim of the present study was to investigate the effects of Epo-D on neointimal hyperplasia using an in vivo rat carotid artery injury model. We demonstrated that local Epo-D treatment significantly reduced neointimal hyperplasia after in vivo rat carotid artery injury, and Epo-D potently inhibited DNA synthesis, cell cycle progression and cell proliferation after FBS- and PDGF-BB-stimulation; PDGF-BB has been identified as the most potent growth factor for stimulating the proliferation of activated rat aortic smooth muscle cells (RASMCs). To clarify the specific effects of Epo-D on cell cycle machinery, we examined its effects on cyclin-dependent kinase (CDK)2, CDK4, cyclin E, p27, and retinoblastoma (Rb) proteins as cell cycle-related proteins in cellular lysates from PDGF-BB-stimulated RASMCs. Epo-D treatment significantly decreased the level of CDK2 protein, but did not change the levels of CDK4 and cyclin E proteins. Furthermore, Epo-D inhibited the phosphorylation of Rb, a key regulator of the G1 to S phase transition in the cell cycle. These findings suggest that Epo-D may regulate the cell cycle G1-checkpoint proteins as its major molecular mechanism for inhibiting neointimal hyperplasia after in vivo rat carotid artery injury.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cdk2 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Cdk4 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin-Dependent Kinase 2,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin-Dependent Kinase 4,
http://linkedlifedata.com/resource/pubmed/chemical/Epothilones,
http://linkedlifedata.com/resource/pubmed/chemical/Platelet-Derived Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Thymidine,
http://linkedlifedata.com/resource/pubmed/chemical/desoxyepothilone B,
http://linkedlifedata.com/resource/pubmed/chemical/platelet-derived growth factor BB
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1537-1891
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pubmed:author |
pubmed-author:AveryMitchell AMA,
pubmed-author:HongJin TaeJT,
pubmed-author:JinYong-RiYR,
pubmed-author:JungJae-ChulJC,
pubmed-author:KimDong-WoonDW,
pubmed-author:KimTack-JoongTJ,
pubmed-author:KwonJin-SookJS,
pubmed-author:SonDong JuDJ,
pubmed-author:SonJu-HeeJH,
pubmed-author:YuinP NPN,
pubmed-author:YunYeo-PyoYP
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pubmed:issnType |
Print
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pubmed:volume |
47
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
229-37
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:17706465-Animals,
pubmed-meshheading:17706465-Carotid Artery Injuries,
pubmed-meshheading:17706465-Cyclin-Dependent Kinase 2,
pubmed-meshheading:17706465-Cyclin-Dependent Kinase 4,
pubmed-meshheading:17706465-Epothilones,
pubmed-meshheading:17706465-G1 Phase,
pubmed-meshheading:17706465-Hyperplasia,
pubmed-meshheading:17706465-Male,
pubmed-meshheading:17706465-Muscle, Smooth, Vascular,
pubmed-meshheading:17706465-Platelet-Derived Growth Factor,
pubmed-meshheading:17706465-Rats,
pubmed-meshheading:17706465-Rats, Sprague-Dawley,
pubmed-meshheading:17706465-Thymidine,
pubmed-meshheading:17706465-Tunica Intima
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pubmed:year |
2007
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pubmed:articleTitle |
Epothilone D, a microtubule-stabilizing compound, inhibits neointimal hyperplasia after rat carotid artery injury by cell cycle arrest via regulation of G1-checkpoint proteins.
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pubmed:affiliation |
College of Pharmacy, Research Center for Bioresource and Health, Chungbuk National University, 12 Gaesin-Dong, Heungduk-Gu, Cheongju 361-763, Republic of Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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