On the identification and biological properties of prostaglandin J2

Abstract Prostaglandin 02 spontaneously decomposes at physiological pH and temperature to 9-deoxy- Δ 9 -PGD 2 (designated PGJ 2 ). We developed a TLC procedure for the isolation of PGJ 2 which was identified by both proton-NMR and mass spectrometry. Freshly prepared PGJ 2 was active in inhibiting aggregation induced by ADP in citrated human platelet rich plasma. As reported by Fukushima et al. (1), PGJ 2 was less active (× 0.1-0.25) than P602 as an inhibitor. Concentrations of PGJ 2 that markedly inhibited aggregation of human platelets were generally incapable of inhibiting aggregation of rat or guinea pig platelets. Using a heterologous system of human platelets mixed with guinea pig plasma samples (2), it was shown that the ability of PGJ 2 to inhibit platelet aggregation was lost immediately following intravenous injection in anesthetized guinea pigs. This apparent rapid uptake and/or degradation of PGJ 2 might also explain why PGJ 2 had no effect on blood pressure of anesthetized guinea pigs. PGJ 2 was potent in inhibiting proliferation of cultured vascular smooth muscle cells, mouse melanoma cells and mouse fibroblasts. Less potent anti-proliferative effects were seen with two other degradation products of PGD 2 , one of which was the δ 12 metabolite reported (3,4) to be formed from PGJ 2 in a reaction catalyzed by serum albumin.