FTY720 Inhibits Tumor Necrosis Factor-alpha-Induced Proliferation and Extracellular Signal-Regulated Kinase Phosphorylation of Human Smooth Muscle Cells

Transplant Proc. 2009 Mar;41(2):705-6. doi: 10.1016/j.transproceed.2008.12.017.

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

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Division / drug effects
  • Cell Survival / drug effects
  • Cells, Cultured
  • Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors*
  • Fingolimod Hydrochloride
  • Graft Rejection / prevention & control*
  • Humans
  • Immunosuppressive Agents / pharmacology*
  • Immunosuppressive Agents / therapeutic use
  • Muscle, Smooth / cytology
  • Muscle, Smooth / drug effects
  • Muscle, Smooth / enzymology
  • Muscle, Smooth / physiology*
  • Phosphorylation
  • Propylene Glycols / pharmacology*
  • Propylene Glycols / therapeutic use
  • Signal Transduction / drug effects
  • Signal Transduction / physiology
  • Sphingosine / analogs & derivatives*
  • Sphingosine / pharmacology
  • Sphingosine / therapeutic use
  • Transplantation, Homologous / immunology
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*
  • Tumor Necrosis Factor-alpha / physiology

Substances

  • Immunosuppressive Agents
  • Propylene Glycols
  • Tumor Necrosis Factor-alpha
  • Extracellular Signal-Regulated MAP Kinases
  • Fingolimod Hydrochloride
  • Sphingosine