11-Keto-9(E),12(E)-octadecadienoic acid, a novel fatty acid that enhances fibrinolytic activity of endothelial cells.
نویسندگان
چکیده
the regulation of fibrinolysis in the blood vessel by producing plasminogen activators and plasminogen activator inhibitors. Defects in physiological regulation of the balance of the activities between plasminogen activator and the inhibitors may cause vascular diseases such as thromboembolismand atherosclerosis. In patients with such diseases, the inhibitor may be dominant in this balance. Actually, the expression of plasminogen activator inhibitor-1 is increased in atherosclerotic arteries1~3), and elevated levels of the inhibitor are
منابع مشابه
Inhibition of plasminogen activator inhibitor-1 by 11-keto-9(E),12(E)-octadecadienoic acid, a novel fatty acid produced by Trichoderma sp.
We have recently found a novel fatty acid, 11-keto-9(E),12(E)-octadecadienoic acid (KOD), that enhances fibrinolytic activity of endothelial cells. The mechanism of action of KOD has been investigated. KOD increased 2-fold the plasmin activity of bovine aortic endothelial cells at 250 microM. The stimulation was dependent on plasminogen and was inhibited by anti-urokinase, whereas KOD did not e...
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We have carried out a study of the reaction of 13Irydroperoxy-9-cis, 11-trans-octadecadienoic acid (linoleic acid hydroperoxide) with hematin. The major products are erythro-ll-hydroxy-l2,13-epoxy-S-octadecenoic acid, threo11-hydroxy12,13-epoxy-9-0~tadecenoic acid, 9,12,13-trihydroxy-lO-octadecenoic acid, 13-keto-9,ll-octadecadienoic acid, and 13-hydroxy-9,ll-octadecadienoic acid. Several minor...
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Background and Objective: Atheroma formation and progression of atherosclerosis are dependent on the expression of bone matrix proteins and regulatory factors such as osteonectin in the vessel walls. Studies have shown that consumption of Trans fatty acids increase risk of cardiovascular diseases. In this study, the effect of elaidic acid on osteonectin gene expression as one of the vascular ca...
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عنوان ژورنال:
- The Journal of antibiotics
دوره 52 2 شماره
صفحات -
تاریخ انتشار 1999