AJP - Cell Physiology, Vol 257, Issue 3 C512-C519, Copyright © 1989 by American Physiological Society
Dexamethasone effects on microvascular endothelial cell lipid composition
M. S. Medow, L. Intrieri, T. Moatter and M. E. Gerritsen
Department of Pediatrics, New York Medical College, Valhalla 10595.
Previous studies have shown that treatment of cultured rabbit coronary
microvessel endothelial (RCME) cells with dexamethasone results in a dose-,
time-, and glucocorticoid-dependent inhibition of prostaglandin release. In
the present study, the effects of dexamethasone on RCME membrane lipid
composition and release of arachidonic acid were examined. This study
demonstrated that dexamethasone treatment did not significantly alter the
relative distribution of membrane phospholipids but did result in changes
of fatty acid composition. There was an increase in saturated and
monounsaturated fatty acids and a decrease in polyunsaturated fatty acids.
Dexamethasone treatment did not reduce A23187-stimulated arachidonic acid
release, despite inhibiting prostaglandin release by 50%. Studies with
radiolabeled arachidonic acid suggest that dexamethasone may exert some
actions on membrane remodeling, an effect that will require further
investigation. Our data strongly suggest that the inhibitory actions of
glucocorticoids on prostaglandin release in cultured RCME cells are not the
result of a generalized inhibition of arachidonic acid release, and
alternate mechanisms must therefore be considered.
