Benidipine, a Calcium Channel Blocker, Regulates Proliferation and Phenotype of Vascular Smooth Muscle Cells
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- Arakawa Emi
- Pharmaceutical Research Center, Kyowa Hakko Kogyo Co., Ltd., Japan
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- Hasegawa Kazuhide
- Pharmaceutical Research Center, Kyowa Hakko Kogyo Co., Ltd., Japan
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Hyperproliferation of phenotypically modified vascular smooth muscle cells (VSMCs) is one of the major factors in the development of atherosclerosis and restenosis. Previously it was demonstrated that benidipine, a dihydropyridine-calcium channel antagonist, reduced neointimal formation in a rat balloon-injury model. In the present study, we examined the effect of benidipine on the phenotypic modulation and proliferation of VSMCs, using primary cultures of rat VSMCs. In the absence of drug treatment, protein levels of the smooth muscle specific markers, such as smooth muscle myosin heavy chain-1 (SM1), calponin 1, and α-actin, decreased during culture. However, treatment of VSMCs with benidipine (3 – 10 μmol/L) for 1 week reversed the effect in a concentration-related manner so that high levels of marker proteins were maintained. The expression of calponin mRNAs was reduced markedly during 1-week culture, and treatment with benidipine (3 μmol/L) significantly inhibited the reduction. Treatment with benidipine for 2 days increased the level of p21 protein and partially reduced p70 S6 kinase 1 (p70S6K1) activity. These data suggest that benidipine may arrest the growth of VSMCs, thereby preventing cell dedifferentiation. These additional properties of benidipine suggest that the drug should provide useful therapy for atherosclerosis and restenosis.<br>
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 100 (2), 149-156, 2006
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390282680154287232
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- NII論文ID
- 10018240794
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- NII書誌ID
- AA11806667
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 7821876
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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
- NDL
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