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The ability of arterial smooth muscle cells (SMC) to produce prostacyclin (PGI2) is well documented both in vivo and under culture conditions. Advanced atherosclerosis has been associated with a severe decrease in PGI2 synthesis by arteries and we recently demonstrated that PGI2 synthesis by cultured SMC from atherosclerotic aorta was significantly depressed. In the present experiments, changes in arachidonic acid (AA) cascade in cultured SMC were studied as a function of cell proliferation and ageing.  SMC derived from explants of the medial layer of 2 years old rabbit aorta were grown under standard conditions (HAM F10 medium + 10 % Foetal Calf Serum). Prostaglandin synthetic activity was investigated by cell free homogenate radiochemical assays and confirmed by gaz chromatography - mass spectrometry determinations after 10 mn incubation with 2 nM AA.  An age related decrease in PGI2 biosynthetic activity (expressed as pM/10PGI6 cells) was found in confluent cells from passages 5 to 22 (31.4 ± 3 vs 15.4 ± 5.6 respectively - p≤0,01 -). On the contrary, PGI2 generation was enhanced during the proliferative phase (day 2-5) (55.5 ± 11.8) when compared to confluent cells at the same (5th) passage (p≤0,01).  These results are consistent with the enhanced PGI2 formation in early arterial proliferative lesion and the inhibition of SMC proliferation by cyclooxygenase inhibitors recently reported and indicate that PGI2 synthetic activity in arterial SMC may be a significant age-dependant endogenous factor involved in the pathogenesis of atherosclerosis.

Prostacyclin Synthesis By Cultured Vascular Smooth Muscle Cells : Influence Of Growth And Ageing