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

Abstract We investigated the effects of the sphingolipid FTY720 on tumor necrosis factor-α (TNF-α)-induced proliferation and signal transduction in human smooth muscle cells (SMC). We showed that clinically relevant concentrations of FTY720 inhibited TNF-α-induced SMC proliferation and extracellular...

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Veröffentlicht in:	Transplantation proceedings 2009-03, Vol.41 (2), p.705-706
Hauptverfasser:	Böhler, T, Kamar, N, Etienne, L, Galvani, S, Canivet, C, Thomsen, M, Salvayre, R, Nègre-Salvayre, A, Rostaing, L, Auge, N
Format:	Artikel
Sprache:	eng
Schlagworte:	Biological and medical sciences Cell Division - drug effects Cell Survival - drug effects Cells, Cultured Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors Fingolimod Hydrochloride Fundamental and applied biological sciences. Psychology Fundamental immunology Graft Rejection - prevention & control Humans Immunology Immunosuppressive Agents - pharmacology Immunosuppressive Agents - therapeutic use Life Sciences Medical sciences 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 Surgery Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Tissue, organ and graft immunology Transplantation, Homologous - immunology Tumor Necrosis Factor-alpha - antagonists & inhibitors Tumor Necrosis Factor-alpha - physiology
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Zusammenfassung:	Abstract We investigated the effects of the sphingolipid FTY720 on tumor necrosis factor-α (TNF-α)-induced proliferation and signal transduction in human smooth muscle cells (SMC). We showed that clinically relevant concentrations of FTY720 inhibited TNF-α-induced SMC proliferation and extracellular signal-regulated kinase (ERK) phosphorylation. We concluded that FTY720 may be a useful drug to inhibit chronic vascular rejection.
ISSN:	0041-1345 1873-2623 0041-1345
DOI:	10.1016/j.transproceed.2008.12.017