Resumen
In rat brain astroglia-enriched cultures long-term treatment with interleukin-1β induces NO release and stimulation of soluble guanylyl cyclase. The cGMP formed is recovered in the extracellular medium but not in the cell monolayer. The interleukin-1β effect is mediated by type I receptor and potentiated by interferon-γ. In cells treated with bacterial endotoxin a larger NO-dependent cGMP accumulation occurs only intracellularly, however a significant cGMP egression is observed when cells are co-treated with interleukin-1β. The non-selective anion transport inhibitors probenecid and verapamil block cGMP efflux, indicating that interleukin-1β stimulates a cGMP transporter. © 2001 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.
Idioma original | Inglés |
---|---|
Páginas (desde-hasta) | 303-306 |
Publicación | FEBS Letters |
Volumen | 507 |
N.º | 3 |
DOI | |
Estado | Publicada - 2 nov 2001 |