Tocopherols and 6-Hydroxy-chroman-2-Carbonitrile Derivatives Inhibit Vascular Smooth Muscle Cell Proliferation by a Nonantioxidant Mechanism

doi:10.1006/abbi.1995.1226

Archives of Biochemistry and Biophysics

Volume 318, Issue 1, 10 May 1995, Pages 241-246

https://doi.org/10.1006/abbi.1995.1226 Get rights and content

Abstract

The effects of two groups of similar compounds, a series of tocopherols and one of 6-hydroxy-chroman-2-carbonitrile, have been studied in vascular smooth muscle cells. A poor correlation has been found between antiproliferative and antioxidant properties of these molecules. D-α-Tocopherol inhibits cell proliferation, while D-α-tocopherylquinone has been found neither to inhibit nor to activate. D-β-Tocopherol, a poor inhibitor of smooth muscle cell proliferation, has been shown to be capable of preventing and reversing the inhibition by D-α-tocopherol. It is concluded that the tocopherols and carbonitrile derivatives tested here appear to inhibit smooth muscle cell proliferation by a nonantioxidant mechanism. The competition between D-α-tocopherol and D-β-tocopherol suggests the existence of a common binding site for the two molecules.

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As proliferation of vascular SMCs is essential for the formation of intimal hyperplasia, inhibition of proliferation of these cells could help to diminish the progression. Studies have shown that vitamin E specifically inhibits rat and human SMC proliferation at physiological concentration, and this occurs via inhibition of PKC activity, one of the important elements in signal transduction cascades [36–38]. Previous studies by our group have shown that, vitamin E prevents cholesterol-induced atherosclerotic lesions in rabbits via inhibition of PKC [13] and CD36 [14] activity.
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Regular ArticleTocopherols and 6-Hydroxy-chroman-2-Carbonitrile Derivatives Inhibit Vascular Smooth Muscle Cell Proliferation by a Nonantioxidant Mechanism

Abstract

Regular Article
Tocopherols and 6-Hydroxy-chroman-2-Carbonitrile Derivatives Inhibit Vascular Smooth Muscle Cell Proliferation by a Nonantioxidant Mechanism