Azelnidipine, a new long-acting calcium-channel blocker, inhibits tumour necrosis factor-α-induced monocyte chemoattractant protein-1 expression in endothelial cells

T. Matsui, Shoichi Yamagishi, K. Nakamura, Hiroyoshi Inoue

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Dihydropyridine-based calcium antagonists are among the most widely used drugs for the treatment of hypertension. Since azelnidipine is a highly lipid-soluble dihydropyridine-based calcium antagonist with high vascular affinity, it is conceivable that azelnidipine could play a protective role against atherosclerosis. The aim of this study was to determine whether azelnidipine could suppress the expression of monocyte chemoattractant protein-1, a principal chemokine which mediates the recruitment of monocytes to the vasculature, in tumour necrosis factor (TNF)-α-exposed human umbilical vein endothelial cells. TNF-α, at a concentration of 10 ng/ml, upregulated monocyte chemoattractant protein-1 mRNA levels about seven-fold. Azelnidipine, 10 nmol/l, was found to inhibit the TNF-α-induced upregulation of monocyte chemoattractant protein-1 mRNA levels in human umbilical vein endothelial cells significantly. Furthermore, azelnidipine suppressed TNF-α-induced monocyte chemoattractant protein-1 production by human umbilical vein endothelial cells. This study demonstrates a novel beneficial aspect of azelnidipine, whereby azelnidipine could play a protective role against atherosclerosis by suppressing monocyte chemoattractant protein-1 overexpression in endothelial cells.

Original languageEnglish
Pages (from-to)671-675
Number of pages5
JournalJournal of International Medical Research
Volume34
Issue number6
Publication statusPublished - 2006 Nov
Externally publishedYes

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Chemokine CCL2
Endothelial cells
Calcium Channel Blockers
Endothelial Cells
Tumor Necrosis Factor-alpha
Human Umbilical Vein Endothelial Cells
Atherosclerosis
Calcium
Messenger RNA
azelnidipine
Chemokines
Blood Vessels
Monocytes
Up-Regulation
Hypertension
Lipids
Pharmaceutical Preparations

Keywords

  • Atherosclerosis
  • Azelnidipine
  • Dihydropyridine-based calcium antagonists
  • Monocyte chemoattractant protein-1
  • Oxidative stress

ASJC Scopus subject areas

  • Medicine(all)

Cite this

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title = "Azelnidipine, a new long-acting calcium-channel blocker, inhibits tumour necrosis factor-α-induced monocyte chemoattractant protein-1 expression in endothelial cells",
abstract = "Dihydropyridine-based calcium antagonists are among the most widely used drugs for the treatment of hypertension. Since azelnidipine is a highly lipid-soluble dihydropyridine-based calcium antagonist with high vascular affinity, it is conceivable that azelnidipine could play a protective role against atherosclerosis. The aim of this study was to determine whether azelnidipine could suppress the expression of monocyte chemoattractant protein-1, a principal chemokine which mediates the recruitment of monocytes to the vasculature, in tumour necrosis factor (TNF)-α-exposed human umbilical vein endothelial cells. TNF-α, at a concentration of 10 ng/ml, upregulated monocyte chemoattractant protein-1 mRNA levels about seven-fold. Azelnidipine, 10 nmol/l, was found to inhibit the TNF-α-induced upregulation of monocyte chemoattractant protein-1 mRNA levels in human umbilical vein endothelial cells significantly. Furthermore, azelnidipine suppressed TNF-α-induced monocyte chemoattractant protein-1 production by human umbilical vein endothelial cells. This study demonstrates a novel beneficial aspect of azelnidipine, whereby azelnidipine could play a protective role against atherosclerosis by suppressing monocyte chemoattractant protein-1 overexpression in endothelial cells.",
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T1 - Azelnidipine, a new long-acting calcium-channel blocker, inhibits tumour necrosis factor-α-induced monocyte chemoattractant protein-1 expression in endothelial cells

AU - Matsui, T.

AU - Yamagishi, Shoichi

AU - Nakamura, K.

AU - Inoue, Hiroyoshi

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AB - Dihydropyridine-based calcium antagonists are among the most widely used drugs for the treatment of hypertension. Since azelnidipine is a highly lipid-soluble dihydropyridine-based calcium antagonist with high vascular affinity, it is conceivable that azelnidipine could play a protective role against atherosclerosis. The aim of this study was to determine whether azelnidipine could suppress the expression of monocyte chemoattractant protein-1, a principal chemokine which mediates the recruitment of monocytes to the vasculature, in tumour necrosis factor (TNF)-α-exposed human umbilical vein endothelial cells. TNF-α, at a concentration of 10 ng/ml, upregulated monocyte chemoattractant protein-1 mRNA levels about seven-fold. Azelnidipine, 10 nmol/l, was found to inhibit the TNF-α-induced upregulation of monocyte chemoattractant protein-1 mRNA levels in human umbilical vein endothelial cells significantly. Furthermore, azelnidipine suppressed TNF-α-induced monocyte chemoattractant protein-1 production by human umbilical vein endothelial cells. This study demonstrates a novel beneficial aspect of azelnidipine, whereby azelnidipine could play a protective role against atherosclerosis by suppressing monocyte chemoattractant protein-1 overexpression in endothelial cells.

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