The lupus anticoagulant stimulates the release of prostacyclin from human endothelial cells.
Decreased endothelial cell production of prostacyclin (PGI2) in response to the lupus anticoagulant has been previously demonstrated and postulated to have a causal relationship to the thrombotic events associated with the lupus anticoagulant. Five patients who exhibited the anticoagulant were studied in an effort to determine if a relationship exists between exposure of endothelial cells to the lupus anticoagulant and decreased production of PGI2. Human endothelial cells derived from human umbilical vein grown in culture were exposed to IgG fractions of patient plasmas containing the lupus anticoagulant. PGI2 released per 10(6) cells was determined by radioimmunoassay for 6-keto-PGF-1-alpha. The overall means for the patient and control groups are given by 47 pM/10(6) cells and 12 pM/10(6) cells respectively. This is a statistically significant difference (F = 10.65, p = 0.017) when the effects of different batches of endothelial cells and thrombin stimulation are adjusted for in the analysis of variance model. These results demonstrate that in this homologous human system exposure of endothelial cells to the lupus anticoagulant leads to stimulation rather than inhibition of PGI2 release.
D015121:6-Ketoprostaglandin F1 alpha / Q000032:analysis; D001779:Blood Coagulation Factors / Q000276:immunology* / Q000502:physiology; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000378:metabolism*; D011464:Epoprostenol / Q000096:biosynthesis*; D006801:Humans; D016682:Lupus Coagulation Inhibitor
D001779:Blood Coagulation Factors; D016682:Lupus Coagulation Inhibitor; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol