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New Mechanism of Rosiglitazone to Reduce Neointimal Hyperplasia Activation of Glycogen Synthase Kinase-3 beta Followed by Inhibition of MMP-9
DC Field | Value | Language |
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dc.contributor.author | Lee, Choon-Soo | - |
dc.contributor.author | Kwon, Yoo-Wook | - |
dc.contributor.author | Yang, Han-Mo | - |
dc.contributor.author | Kim, Sung-Hwan | - |
dc.contributor.author | Hur, Jin | - |
dc.contributor.author | Cho, Hyun-Jai | - |
dc.contributor.author | Park, Young-Bae | - |
dc.contributor.author | Kim, Hyo-Soo | - |
dc.contributor.author | Kang, Hyun-Jae | - |
dc.contributor.author | Park, Kyung-Woo | - |
dc.contributor.author | Kim, Tae-Youn | - |
dc.date.accessioned | 2012-06-26T00:31:20Z | - |
dc.date.available | 2012-06-26T00:31:20Z | - |
dc.date.issued | 2009-04 | - |
dc.identifier.citation | ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY; Vol.29 4; 472-479 | ko_KR |
dc.identifier.issn | 1079-5642 | - |
dc.identifier.uri | https://hdl.handle.net/10371/77411 | - |
dc.description.abstract | Objective-Mechanism of neointimal hyperplasia after vascular injury includes activation of signaling pathways and matrix metalloproteinases (MMPs) that are involved in cell proliferation and migration. Rosiglitazone, a synthetic peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonist, was reported to inhibit neointimal hyperplasia in diabetic animals and humans. But the underlying mechanism has not been clarified. In this study, we examined how rosiglitazone inhibited neointimal hyperplasia. Methods and Results-The proliferation and survival of cultured rat VSMCs were reduced by rosiglitazone, which was mediated by inhibition of ERK and activation GSK-3 beta, without change of Akt. The antiproliferative effect of rosiglitazone was reversed by GSK-3 beta inactivation. The migration of VSMCs was also suppressed by rosiglitazone that inhibited the expression and activity MMP-9 through GSK-3 beta activation. Thus migration of MMP-9(-/-) VSMCs from MMP-9 knockout mice was not affected by rosiglitazone. The underlying mechanism of MMP-9 suppression by rosiglitazone was that it inhibited NF-kappa B DNA binding activity, which was also dependent on GSK-3 beta. In rat carotid artery, balloon injury significantly inactivated GSK-3 beta with induction of MMP-9, which was effectively prevented by rosiglitazone. Thus, rosiglitazone significantly decreased the ratio of intima to media by reducing proliferation and inducing apoptosis of VSMCs at neointima, which was reversed by inactivation of GSK-3 beta with adenoviral transfer of catalytically-inactive GSK-KM gene. Conclusions-Rosiglitazone activates GSK-3 beta, which inhibits not only proliferation of VSMCs but also migration of VSMCs through blocking NF-kappa B-dependent MMP-9 activation. (Arterioscler Thromb Vasc Biol. 2009; 29: 472-479.) | ko_KR |
dc.description.sponsorship | This study was supported by grants from the National Research
Laboratory of Cardiovascular Stem Cell and the Innovative Research Institute for Cell Therapy (A062260), Republic of Korea. | ko_KR |
dc.language.iso | en | ko_KR |
dc.publisher | LIPPINCOTT WILLIAMS & WILKINS | ko_KR |
dc.subject | restenosis | ko_KR |
dc.subject | rosiglitazone | ko_KR |
dc.subject | VSMCs | ko_KR |
dc.subject | MMP-9 | ko_KR |
dc.subject | GSK-3 beta | ko_KR |
dc.title | New Mechanism of Rosiglitazone to Reduce Neointimal Hyperplasia Activation of Glycogen Synthase Kinase-3 beta Followed by Inhibition of MMP-9 | ko_KR |
dc.type | Article | ko_KR |
dc.contributor.AlternativeAuthor | 이준수 | - |
dc.contributor.AlternativeAuthor | 권유욱 | - |
dc.contributor.AlternativeAuthor | 양한모 | - |
dc.contributor.AlternativeAuthor | 김성환 | - |
dc.contributor.AlternativeAuthor | 김태윤 | - |
dc.contributor.AlternativeAuthor | 허진 | - |
dc.contributor.AlternativeAuthor | 박경우 | - |
dc.contributor.AlternativeAuthor | 조현재 | - |
dc.contributor.AlternativeAuthor | 강현재 | - |
dc.contributor.AlternativeAuthor | 박영배 | - |
dc.contributor.AlternativeAuthor | 김효수 | - |
dc.identifier.doi | 10.1161/ATVBAHA.108.176230 | - |
dc.citation.journaltitle | ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY | - |
dc.description.citedreference | Mitra AK, 2006, J CLIN PATHOL, V59, P232, DOI 10.1136/jcp.2005.025742 | - |
dc.description.citedreference | Jonas M, 2005, CIRC RES, V97, P725, DOI 10.1161/01.RES.0000183730.52908.C6 | - |
dc.description.citedreference | Feinstein DL, 2005, BIOCHEM PHARMACOL, V70, P177, DOI 10.1016/j.bcp.2005.03.033 | - |
dc.description.citedreference | Redondo S, 2005, DIABETES, V54, P811 | - |
dc.description.citedreference | Gennaro G, 2004, CIRCULATION, V110, P3367, DOI 10.1161/01.CIR.0000147773.86866.CD | - |
dc.description.citedreference | Choi D, 2004, DIABETES CARE, V27, P2654 | - |
dc.description.citedreference | Chung TW, 2004, FASEB J, V18, P1670, DOI 10.1096/fj.04-2126com | - |
dc.description.citedreference | Yang HM, 2004, CIRCULATION, V110, P301, DOI 10.1161/01.CIR.0000135467.43430.16 | - |
dc.description.citedreference | Marx N, 2004, CIRC RES, V94, P1168, DOI 10.1161/01.RES.0000127122.22685.0A | - |
dc.description.citedreference | Osman A, 2004, AM HEART J, V147, DOI 10.1016/j.ahj.2003.12.006 | - |
dc.description.citedreference | Moon SK, 2004, J CELL PHYSIOL, V198, P417, DOI 10.1002/jcp.10435 | - |
dc.description.citedreference | Tao L, 2003, CIRCULATION, V108, P2805, DOI 10.1161/01.CIR.0000097003.49585.5E | - |
dc.description.citedreference | Stabile E, 2003, CIRC RES, V93, P1059, DOI 10.1161/01.RES.0000105086.31909.1B | - |
dc.description.citedreference | Phillips JW, 2003, CIRCULATION, V108, P1994, DOI 10.1161/01.CIR.0000092886.52404.50 | - |
dc.description.citedreference | Park KW, 2003, ARTERIOSCL THROM VAS, V23, P1364, DOI 10.1161/01.ATV.0000081633.53390.B4 | - |
dc.description.citedreference | Moon SK, 2003, BIOCHEM BIOPH RES CO, V301, P1069, DOI 10.1016/S0006-291X(03)00091-3 | - |
dc.description.citedreference | Liu DY, 2003, FERTIL STERIL, V79, P74 | - |
dc.description.citedreference | DESOUZA CV, 2003, J CARDIOVASC PHARM T, V8, P297 | - |
dc.description.citedreference | Sutton MS, 2002, DIABETES CARE, V25, P2058 | - |
dc.description.citedreference | Kim HS, 2002, J BIOL CHEM, V277, P41888, DOI 10.1074/jbc.M206657200 | - |
dc.description.citedreference | Barbier O, 2002, ARTERIOSCL THROM VAS, V22, P717, DOI 10.1161/01/ATV.0000015598.86369.04 | - |
dc.description.citedreference | Mayerson AB, 2002, DIABETES, V51, P797 | - |
dc.description.citedreference | Izumi Y, 2001, CIRC RES, V88, P1120 | - |
dc.description.citedreference | Kodera Y, 2000, J BIOL CHEM, V275, P33201 | - |
dc.description.citedreference | Law RE, 2000, CIRCULATION, V101, P1311 | - |
dc.description.citedreference | Mason DP, 1999, CIRC RES, V85, P1179 | - |
dc.description.citedreference | Dollery CM, 1999, CIRCULATION, V99, P3199 | - |
dc.description.citedreference | Marx N, 1998, AM J PATHOL, V153, P17 | - |
dc.description.citedreference | Hu YH, 1997, ARTERIOSCL THROM VAS, V17, P2808 | - |
dc.description.citedreference | SACHINIDIS A, 1995, HYPERTENSION, V26, P771 | - |
dc.description.citedreference | TRAENCKNER EBM, 1995, EMBO J, V14, P2876 | - |
dc.description.citedreference | KITAZONO T, 1995, CIRCULATION, V91, P1129 | - |
dc.description.citedreference | BAEUERLE PA, 1988, SCIENCE, V242, P540 | - |
dc.description.citedreference | DEBIASIO R, 1987, J CELL BIOL, V105, P1613 | - |
dc.description.tc | 17 | - |
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