Cyclooxygenase-2 mediates platelet-activating factor-induced prostaglandin E2 release from rat primary astrocytes

• Published in: Neuroscience letters 2003-04, Vol.340 (3), p.177-180
• Main Authors: TEATHER, Lisa A, WURTMAN, Richard J
• Format: Article
• Language: English
• Subjects: Animals; Astrocytes - drug effects; Astrocytes - enzymology; Astrocytes - metabolism; Biological and medical sciences; Cells, Cultured; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors - pharmacology; Dinoprostone - metabolism; Fundamental and applied biological sciences. Psychology; Isoenzymes - antagonists & inhibitors; Isoenzymes - physiology; Isolated neuron and nerve. Neuroglia; Platelet Activating Factor - metabolism; Platelet Activating Factor - pharmacology; Prostaglandin-Endoperoxide Synthases - physiology; Rats; Vertebrates: nervous system and sense organs
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/S0304-3940(03)00129-0

The phospholipid mediator platelet-activating factor (PAF), and its non-hydrolyzable analog methylcarbamyl-PAF (mc-PAF) increase prostaglandin E(2) (PGE(2)) release from astrocyte-enriched cortical cell cultures. Cyclooxygenase (COX) enzymes--of which there are two known isoforms--convert arachidonic acid to prostaglandin (PG) H(2) (PGH(2)), which is further metabolized to various PGs, including PGE(2). COX-1 is generally considered to contribute to cell homeostasis, whereas COX-2 is thought to mediate inflammatory/immune PG formation. In this study we examined the involvement of the COX isoforms in PAF-induced PGE(2) release. Treatment of cells with the non-specific COX inhibitor indomethacin, or the specific COX-2 inhibitor NS-398, prior to mc-PAF stimulation completely blocked the PAF-induced release of PGE(2); treatment with more selective COX-1 inhibitors (i.e. piroxicam and SC-560) failed to significantly do so. These data suggest that COX-2 is responsible for PAF-mediated PGE(2) release in primary astrocytes.