Abstract
GbaSM-4 cells, vascular smooth muscle cells (VSMCs) derived from brain basilar arteries, were shown to migrate toward d-nicotine by augmenting the actin cytoskeleton in their cell bodies and lamellipodia, and expression of nicotinic acetylcholine receptor (alpha7-nAChR) was detected in GbaSM-4 cells. Their chemotaxis was antagonized by an alpha7-nAChR antagonist of methyllycaconitine. It was also antagonized by inhibiting myosin light chain (MLC) kinase and by down-regulating MLC kinase. However, the changes in MLC phosphorylation were not associated with the nicotine treatment, suggesting the involvement of non-kinase activity of MLC kinase as reviewed by Gao et al. (IUBMB Life. 2001;51:337). This plot may work to induce arteriosclerosis during cigarette smoking.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Aconitine / analogs & derivatives*
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Aconitine / antagonists & inhibitors
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Aconitine / pharmacology
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Actins / metabolism
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Animals
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Basilar Artery / cytology
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Cell Line
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Chemotaxis / drug effects
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Chemotaxis / physiology*
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Cytoskeleton / metabolism
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Down-Regulation / physiology
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Forecasting
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Guinea Pigs
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Muscle, Smooth, Vascular / cytology
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Muscle, Smooth, Vascular / metabolism*
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Myosin-Light-Chain Kinase / antagonists & inhibitors
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Myosin-Light-Chain Kinase / metabolism
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Nicotine / metabolism*
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Nicotine / pharmacology
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Phosphorylation
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Pseudopodia / metabolism
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Receptors, Nicotinic / chemistry
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Receptors, Nicotinic / genetics
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Receptors, Nicotinic / metabolism*
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Stereoisomerism
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alpha7 Nicotinic Acetylcholine Receptor
Substances
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Actins
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Receptors, Nicotinic
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alpha7 Nicotinic Acetylcholine Receptor
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methyllycaconitine
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Nicotine
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Myosin-Light-Chain Kinase
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Aconitine