The release of platelet-activating factor from human endothelial cells in culture.
- 1 November 1983
- journal article
- research article
- Published by The American Association of Immunologists in The Journal of Immunology
- Vol. 131 (5), 2397-2403
- https://doi.org/10.4049/jimmunol.131.5.2397
Abstract
The release of platelet-activating factor (PAF) from stimulated human endothelial cells (HEC) cultured from normal term, umbilical cord veins is described. HEC in primary cultures released PAF after challenge with A23187, rabbit anti-human factor VIII (RaHu/FVIII), angiotensin II, and vasopressin. HEC subcultures maintained the ability to release PAF in the presence of A23187 and RaHu/FVIII, whereas the release of PAF in response to angiotensin II and vasopressin was not constant and was reduced. Control cultured, smooth muscle cells derived from umbilical cord veins, previously depleted of endothelial cells, did not release PAF under the above-mentioned stimulation. Plastic-adherent or cultured monocytes released PAF with A23187, but not with RaHu/FVIII, angiotensin II, and vasopressin. The release of PAF from HEC in primary cultures required the presence of extracellular cations and the activation of membrane phospholipase A2. PAF release induced by A23187, RaHu/FVIII, angiotensin II, and vasopressin was unaffected by indomethacin, an inhibitor of cyclooxygenase, which, however, favored the release of PAF from HEC stimulated with thrombin, a stimulus that did not affect HEC in the absence of indomethacin. PGI2 inhibited PAF release from stimulated HEC. The relevance of an acetylation process in the biosynthesis of PAF and HEC was supported by the following evidence: 1) the increase in PAF yield in the presence of sodium acetate and, particularly, of acetyl-CoA; 2) the incorporation of [14C]acetate into PAF molecules; 3) the loss of radioactivity and of biologic activity after treatment with phospholipase A2. These results indicate that HEC in culture are able to release PAF and that metabolic pathways similar to those described for leukocytes are involved.This publication has 26 references indexed in Scilit:
- Enzymatic synthesis of 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine, a hypotensive and platelet-aggregating lipid.Journal of Biological Chemistry, 1980
- Platelet-Activating Factor (PAF-Acether) Secretion from Platelets: Effect of Aggregating AgentsBritish Journal of Haematology, 1980
- Identification of platelet activating factor isolated from rabbit basophils as acetyl glyceryl ether phosphorylcholine.Journal of Biological Chemistry, 1980
- Physical and chemical properties of platelet-activating factor obtained from human neutrophils and monocytes and rabbit neutrophils and basophilsBiochimica et Biophysica Acta (BBA) - General Subjects, 1980
- Physicochemical and Functional Identity of Rabbit Platelet-Activating Factor (PAF) Released in Vivo during IgE Anaphylaxis with PAF Released in Vitro from IgE Sensitized BasophilsThe Journal of Immunology, 1979
- Platelet-activating factor. Evidence for 1-O-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine as the active component (a new class of lipid chemical mediators).Journal of Biological Chemistry, 1979
- Platelet‐activating factor and macrophages. I. Evidence for the release from rat and mouse peritoneal macrophages and not from mastocytesEuropean Journal of Immunology, 1979
- Stimulation of Endothelial Cell Prostacyclin Production by Thrombin, Trypsin, and the Ionophore A 23187JCI Insight, 1978
- Activation of Rabbit Platelets by Platelet-Activating Factor Derived from IgE-Sensitized BasophilsJCI Insight, 1977
- Modulation of human platelet adenylate cyclase by prostacyclin (PGX)Prostaglandins, 1977