0 286

Cited 22 times in

Dominant negative insulin-like growth factor-1 receptor inhibits neointimal formation through suppression of vascular smooth muscle cell migration and proliferation, and induction of apoptosis

DC Field Value Language
dc.contributor.author고영국-
dc.contributor.author장양수-
dc.date.accessioned2020-09-04T02:05:47Z-
dc.date.available2020-09-04T02:05:47Z-
dc.date.issued2004-12-
dc.identifier.issn0006-291X-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/178802-
dc.description.abstractBlocking of the IGF-1 signaling pathway targeting the IGF-1 receptor (IGF-1R) provides a potential treatment strategy for restenosis. In this study, we have examined the effects of a dominant negative IGF-1R (IGF-1Rt) on primary rat VSMCs in vitro and on injured rat carotid artery in vivo. Ad/IGF-1Rt infection inhibited VSMC migration and proliferation, and it also induced apoptosis by inhibiting phosphorylation of Akt and phosphorylation of ERK1/2. Consistent with the anti-proliferative and apoptotic effects in vitro, the Ad/IGF-1Rt infection markedly reduced neointimal formation in carotid injury model. Ad/IGF-1Rt treated carotid arteries exhibited a suppressed proliferation index, PCNA expression, and also were stained positive for TUNEL assay. These results indicate that a dominant negative IGF-1R has the potential to reduce neointimal formation of injured rats' carotid arteries. The delivery of dominant negative IGF-1R by adenoviral or other vectors may provide a useful strategy for inhibiting restenosis after angioplasty.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherElsevier-
dc.relation.isPartOfBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.subject.MESHAngioplasty, Balloon / adverse effects-
dc.subject.MESHAnimals-
dc.subject.MESHApoptosis / drug effects-
dc.subject.MESHApoptosis / genetics-
dc.subject.MESHCell Movement / drug effects-
dc.subject.MESHCell Movement / genetics-
dc.subject.MESHCell Proliferation / drug effects-
dc.subject.MESHCells, Cultured-
dc.subject.MESHCoronary Restenosis / etiology-
dc.subject.MESHCoronary Restenosis / genetics-
dc.subject.MESHCoronary Restenosis / pathology*-
dc.subject.MESHCoronary Restenosis / prevention & control*-
dc.subject.MESHGene Transfer Techniques*-
dc.subject.MESHGenes, Dominant / genetics-
dc.subject.MESHGenetic Therapy / methods-
dc.subject.MESHMale-
dc.subject.MESHMuscle, Smooth, Vascular / drug effects-
dc.subject.MESHMuscle, Smooth, Vascular / physiopathology*-
dc.subject.MESHRats-
dc.subject.MESHRats, Sprague-Dawley-
dc.subject.MESHReceptor, IGF Type 1 / agonists*-
dc.subject.MESHReceptor, IGF Type 1 / genetics*-
dc.subject.MESHTreatment Outcome-
dc.subject.MESHTunica Intima / drug effects-
dc.subject.MESHTunica Intima / growth & development-
dc.subject.MESHTunica Intima / pathology-
dc.titleDominant negative insulin-like growth factor-1 receptor inhibits neointimal formation through suppression of vascular smooth muscle cell migration and proliferation, and induction of apoptosis-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학교실)-
dc.contributor.googleauthorHyun-Joung Lim 1 , Hyun-Young Park, Young-Guk Ko, Sea-Hyoung Lee, Seung-Yeon Cho, Eun Jig Lee, J Larry Jameson, Yangsoo Jang-
dc.identifier.doi10.1016/j.bbrc.2004.10.175-
dc.contributor.localIdA00127-
dc.contributor.localIdA03448-
dc.relation.journalcodeJ00281-
dc.identifier.eissn1090-2104-
dc.identifier.pmid15541402-
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S0006291X04024234-
dc.contributor.alternativeNameKo, Young Guk-
dc.contributor.affiliatedAuthor고영국-
dc.contributor.affiliatedAuthor장양수-
dc.citation.volume325-
dc.citation.number3-
dc.citation.startPage1106-
dc.citation.endPage1114-
dc.identifier.bibliographicCitationBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol.325(3) : 1106-1114, 2004-12-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.