Inhibition of Migration and Proliferation of Rat Vascular Smooth Muscle Cells by a New HMG-CoA Reductase Inhibitor, Pitavastatin.
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- KOHNO Masakazu
- Second Department of Internal Medicine, School of Medicine, Kagawa Medical University
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- SHINOMIYA Kaori
- Second Department of Internal Medicine, School of Medicine, Kagawa Medical University
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- ABE Satomi
- Second Department of Internal Medicine, School of Medicine, Kagawa Medical University
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- NOMA Takahisa
- Second Department of Internal Medicine, School of Medicine, Kagawa Medical University
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- KONDO Isao
- Second Department of Internal Medicine, School of Medicine, Kagawa Medical University
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- OSHITA Akira
- Second Department of Internal Medicine, School of Medicine, Kagawa Medical University
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- TAKEUCHI Hiroto
- Second Department of Internal Medicine, School of Medicine, Kagawa Medical University
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- TAKAGI Yuichiro
- Second Department of Internal Medicine, School of Medicine, Kagawa Medical University
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- YUKIIRI Kazushi
- Second Department of Internal Medicine, School of Medicine, Kagawa Medical University
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- MIZUSHIGE Katsufumi
- Second Department of Internal Medicine, School of Medicine, Kagawa Medical University
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- OHMORI Koji
- Second Department of Internal Medicine, School of Medicine, Kagawa Medical University
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抄録
The migration and proliferation of vascular smooth muscle cells (SMCs) are known to play roles in the pathogenesis of atherosclerosis. Therapy with a reductase inhibitor of 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA)(“statin”) produces significant alterations in various SMC functions. The objectives of the present study were to determine whether pitavastatin, a new chemically synthesized and powerful statin, can affect angiotensin II (Ang II)- and platelet-derived growth factor (PDGF)-induced migration and proliferation of cultured rat vascular SMCs. The effect of pitavastatin on cell viability was also examined in these cells. Migration was evaluated by the Boyden’s chamber method using microchemotaxis chambers. As expected, Ang II and PDGF BB potently stimulated cell migration in a concentration-dependent manner. Pitavastatin significantly inhibited Ang II (10-6mol⁄l)-induced migration at the concentrations of 10-8 and 10-7mol⁄l. Pitavastatin also inhibited PDGF BB (1ng⁄ml)-induced migration at concentrations between 10-9 and 10-8 mol⁄l in a relatively concentration-dependent manner. This statin modestly but significantly inhibited Ang II (10-6 mol⁄l)- and PDGF BB (1 ng⁄ml)-induced DNA synthesis at concentrations between 10-9 and 10-7 mol⁄l. In addition, pitavastatin clearly inhibited Ang II (10-6 mol⁄l)- and PDGF BB (1ng⁄ml)-induced increases of cell number at concentrations between 10-9 and 10-7mol⁄l. Pitavastatin did not affect lactate dehydrogenase release from these cells at the concentrations used in this experiment. In a trypan blue exclusion test, dead cells stained with trypan blue were not found 24 h after treatment with 10-9, 10-8 or 10-7 mol⁄l of pitavastatin. These findings suggest that pitavastatin suppresses the migration and proliferation stimulated by Ang II and PDGF BB without affecting cell viability. Pitavastatin may exert an anti-atherogenic effect, in part, through these mechanisms. (Hypertens Res 2002; 25: 279-285)
収録刊行物
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- Hypertension Research
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Hypertension Research 25 (2), 279-285, 2002
日本高血圧学会
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詳細情報 詳細情報について
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- CRID
- 1390282679696934016
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- NII論文ID
- 130004436977
- 50001105881
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- NII書誌ID
- AA10847079
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- COI
- 1:CAS:528:DC%2BD38XktlOgsbY%3D
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- ISSN
- 13484214
- 09169636
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- PubMed
- 12047044
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可