Effect of endothelium on glycosaminoglycan accumulation in injured rabbit aorta.

Previous studies have indicated that reendothelialized regions of injured rabbit aortas are more susceptible to diet-induced atherosclerosis than persistently deendothelialized regions or uninjured aortas. However, the mechanism responsible for this selective lipid deposition is not understood. One possibility is that these regions differ with respect to the quantity and type of glycosaminoglycan-containing proteoglycans which are known to interact with lipoproteins.

Platelet adhesion to cultured vascular endothelial cells. A quantitative monolayer adhesion assay.

We have developed a sensitive in vitro method for measuring the adherence of platelets to cultured vascular cells. Human platelets, in citrated plasma, were radiolabeled with [3H]adenine to achieve a specific activity 100 to 1000 times greater than that obtainable with chromium-51 or [14C]serotonin. After exposure of cultured cell monolayers to radiolabeled PRP, nonadherent platelets were removed by a standardized wash procedure, and the number of adherent platelets calculated from liquid scintillation measurements.

In vitro studies of thromboresistance: the role of prostacyclin (PGI2) in platelet adhesion to cultured normal and virally transformed human vascular endothelial cells.

Circulating blood platelets normally do not adhere to, or aggregate on, the vascular endothelial lining. We have developed an in vitro model system to study the mechanisms of endothelial resistance to platelet adhesion, and to determine the role of prostacyclin (PGI2) in this process. This system combines scanning electron microscopy and measurement of bound (3H)-adenine-labeled platelets to examine platelet adhesion to primary cultures of human endothelial cells, which generate PGI2-like activity, and to virally transformed endothelial cells, which lack this activity.