Abstract
We investigated the effects of the sphingolipid FTY720 on tumor necrosis factor-alpha (TNF-alpha)-induced proliferation and signal transduction in human smooth muscle cells (SMC). We showed that clinically relevant concentrations of FTY720 inhibited TNF-alpha-induced SMC proliferation and extracellular signal-regulated kinase (ERK) phosphorylation. We concluded that FTY720 may be a useful drug to inhibit chronic vascular rejection.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Cell Division / drug effects
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Cell Survival / drug effects
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Cells, Cultured
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Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors*
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Fingolimod Hydrochloride
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Graft Rejection / prevention & control*
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Humans
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Immunosuppressive Agents / pharmacology*
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Immunosuppressive Agents / therapeutic use
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Muscle, Smooth / cytology
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Muscle, Smooth / drug effects
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Muscle, Smooth / enzymology
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Muscle, Smooth / physiology*
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Phosphorylation
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Propylene Glycols / pharmacology*
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Propylene Glycols / therapeutic use
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Signal Transduction / drug effects
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Signal Transduction / physiology
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Sphingosine / analogs & derivatives*
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Sphingosine / pharmacology
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Sphingosine / therapeutic use
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Transplantation, Homologous / immunology
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Tumor Necrosis Factor-alpha / antagonists & inhibitors*
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Tumor Necrosis Factor-alpha / physiology
Substances
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Immunosuppressive Agents
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Propylene Glycols
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Tumor Necrosis Factor-alpha
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Extracellular Signal-Regulated MAP Kinases
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Fingolimod Hydrochloride
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Sphingosine