Abstract
Prostacyclin and its mimetics have repeatedly been shown to act antiatherogenic and to inhibit neointima formation in several animal models of vascular injury. Treatment of human vascular smooth muscle cells with the prostacyclin mimetic iloprost (100 nm) drastically reduces expression of Cyr61, encoding the growth-regulatory cystein-rich angiogenic protein, without affecting the degradation rate of Cyr61 mRNA. Thrombin-induced Cyr61 expression was inhibited completely in the presence of iloprost. It is concluded that vasoprotective actions of prostacyclin in vivo may in part be due to inhibition of expression of the growth regulatory gene Cyr61 at sites of vascular lesions.
MeSH terms
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Cells, Cultured
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Cysteine-Rich Protein 61
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Down-Regulation / drug effects*
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Down-Regulation / physiology
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Gene Expression Regulation / drug effects*
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Gene Expression Regulation / physiology
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Humans
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Iloprost / pharmacology*
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Immediate-Early Proteins / biosynthesis*
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Immediate-Early Proteins / genetics
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Intercellular Signaling Peptides and Proteins / biosynthesis*
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Intercellular Signaling Peptides and Proteins / genetics
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Muscle, Smooth, Vascular / cytology
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Muscle, Smooth, Vascular / drug effects*
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Muscle, Smooth, Vascular / metabolism
Substances
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CCN1 protein, human
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Cysteine-Rich Protein 61
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Immediate-Early Proteins
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Intercellular Signaling Peptides and Proteins
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Iloprost