Abstract

<h2>Abstract</h2> One batch of human β-thromboglobulin (βTG) was found to inhibit PGI<sub>2</sub> production by pig aortic endothelial cells in culture. PGE<sub>2</sub> production by these cells was also inhibited. βTG had a similar inhibitory effect on prostaglandin production by pig aortic smooth muscle and mouse 3T3 cells and this inhibitory activity was reduced to 50% of control value on Amicon filter dialysis. Three subsequent batches of βTG were found to be without effect on prostaglandin production by aortic endothelium and 3T3 cells. Ammonium acetate and sodium azide, which are used during the preparation of βTG, were tested for inhibitory activity and were active against endothelial cell prostaglandin production only at concentrations that were cytotoxic; these ions were therefore unlikely to account for the inhibitory activity of βTG initially seen. Freshly isolated endothelial cells and subcultured endothelial and smooth muscle cells at different stages of growth to confluence were also tested to see if the previously described βTG receptor had been lost during growth of cells in culture. The effect of γTG or low affinity platelet factor 4 (LA-PF4), the precursor of βTG, was compared with that of βTG. No inhibitory effects of βTG or γTG were found under these conditions. We therefore conclude firstly, that any effects of βTG or γTG on prostaglandin production by vascular cells in culture cannot be reproducibly demonstrated, and secondly, that any such effect is not specific for PGI<sub>2</sub> or for endothelium.

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