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Lipoxins stimulate prostacyclin generation by human endothelial cells
Author(s) -
Brezinski Mark E.,
Gimbrone Michael A.,
Nicolaou K.C.,
Serhan Charles N.
Publication year - 1989
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(89)80214-5
Subject(s) - prostacyclin , chemistry , microbiology and biotechnology , biochemistry , biology
Cultured human umbilical endothelial cells were incubated with lipoxins and their ability to generate prostacyclin (PGI 2 ) was assessed and compared to that induced by either leukotriene C 4 or an ionophore of divalent cations (A‐23,187). When exposed to either lipoxin A 4 , lipoxin B 4 , or 7‐ cis , 11‐ trans ‐lipoxin A 4 , endothelial cells generated prostacyclin detected as 6‐keto‐PGF 1α . Of the lipoxins examined, 7‐ cis , 11‐ trans ‐lipoxin A 4 proved to be the most effective with PGI 2 production twice that induced by equimolar amounts of A‐23,187 (5 μM). On a molar basis, lipoxin A 4 and lipoxin B 4 were less potent than leukotriene C 4 although they were more efficacious. When either lipoxin A 4 or lipoxin B 4 was added to cells simultaneously with leukotriene C 4 , the formation of prostacyclin was greater than that induced by leukotriene C 4 alone. During the time course of exposure to lipoxins (0–20 min, 37°C), cultured endothelial cells did not further transform these compounds via ω‐oxidation as determined by reverse‐phase HPLC. These data indicate that lipoxins can stimulate PGI 2 generation by human endothelial cells. Moreover, they suggest a role for these lipoxygenase products of arachidonic acid in the regulation of hemostasis, inflammation and vascular reactivity.