Arachidonic acid metabolites produced by platelet-depleted human blood monocytes: A possible role in thrombogenesis
✍ Scribed by Dr. C. Michael Jones; Elizabeth R. Hall; Jeanne P. Hester; Kenneth K. Wu
- Publisher
- John Wiley and Sons
- Year
- 1989
- Tongue
- English
- Weight
- 592 KB
- Volume
- 31
- Category
- Article
- ISSN
- 0361-8609
No coin nor oath required. For personal study only.
✦ Synopsis
The arachidonic acid metabolites produced by human peripheral blood monocytes were studied to determine which metabolites could have a role in thrombogenesis. Monocytes were found to be free of platelets by scanning electron microscopy and by measurement of 12-HETE. Human peripheral blood monocytes produce thromboxane as their major metabolite. Thromboxane levels reached a plateau at 12-16 hours of culture. Monocytes produced relatively little prostaglandin E2 or F2. In contrast to our control platelet preparation, neither A23187 (1-10 pM) nor exogenous arachidonic acid (0-40 pM) caused an increase in monocyte thromboxane 82. On the other hand, lipopolysaccharide (20 pg per ml), collagen (2.5 mg per lo7 cells), and thrombin (5-10 units per ml) caused a two-to fivefold increase in monocyte thromboxane 82 in most donors but had no effect on prostaglandin F l a levels. Blockage of thromboxane synthase by 1-benzylimidazole abolished thromboxane B2 production but did not increase prostaglandin F1 a. Finally, aspirin-treated platelets from a volunteer donor, which were refractory to 30 FM arachidonate, could be aggregated by isolated blood monocytes.
Our data indicate that monocytes are capable of producing thromboxane in large amounts. The regulation of this increase, however, appears to be quite different from platelets. We postulate that monocytes may have a role in hemostasis by virtue of their ability to adhere at sites of vascular injury and release thromboxane, which may enhance platelet aggregation and thrombus formation.