Premium
Pro‐inflammatory mediators induce sustained release of prostaglandin E 2 from human dermal microvascular endothelial cells
Author(s) -
BULL HELEN A.,
RUSTIN M.H.A.,
SPAULL J.,
COHEN J.,
WILSONJONES E.,
DOWD PAULINE M.
Publication year - 1990
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.1990.tb08261.x
Subject(s) - prostaglandin e2 , prostacyclin , cycloheximide , prostaglandin , stimulation , erythema , lipopolysaccharide , endocrinology , prostaglandin e , vasodilation , chemistry , medicine , pharmacology , immunology , biochemistry , protein biosynthesis
SUMMARY The vasodilator prostaglandin E 2 has been proposed as a mediator of erythema in a variety of cutaneous inflammatory reactions and prostacyclin levels have been found to be elevated in ultraviolet induced erythema. Human recombinant interleukin i α and lipopolysaccharide induced a concentration‐ and time‐dependent release of prostaglandin E 2 , but not prostacyclin, from cultured neonatal and adult human dermal microvascular endothelial cells. Prostaglandin E 2 was measurable at 2 h after stimulation with i U/ml interleukin Iα, levels increased rapidly up to 6 h and more slowly up to 24 h. Lipopolysaccharide (20 μg/ml) induced measurable release of prostaglandin E 2 between 2 and 4 h after stimulation and release continued up to 24 h when incubation was terminated. With both agonists, release of prostaglandin E2 was inhibited by indomethacin and significantly reduced by cycloheximide. The sensitivity and magnitude of responses of the cutaneous endothelial cells to these pro‐inflammatory stimuli appeared to be dependent on their derivation.