Conjugated Linoleic Acids Exert Similar Actions on Prostanoid Release from Aortic and Coronary Artery Smooth Muscle Cells

Conjugated linoleic acids (CLAs) are biologically active lipid compounds exerting anti-atherogenic actions in vivo without exact knowledge about the underlying mechanisms. Recently, CLAs were shown to lower the release of vasoactive prostanoids from vascular smooth muscle cells (SMCs) which play a central role in atherosclerosis. Since SMCs from different vascular locations were shown to exert differential actions in response to a common stimulus, the present study aimed to explore potential differential effects of CLA isomers on the release of the prostanoids PGE₂ and PGI₂ from coronary artery and aortic SMCs. For this purpose, human aortic and coronary artery SMCs were incubated with 5 and 50 μmol/L of cis-9, trans-11 CLA and trans-10, cis-12 CLA for 24 hours and analyzed for fatty acid composition and the release of prostaglandins E₂ and I₂ (PGE₂ and PGI₂). Incubations were performed in the absence (basal conditions) and in the presence of 10 ng/mL of the cytokine tumor necrosis factor-α (TNFα) (cytokine-stimulated conditions). Fatty acid analysis revealed a similar degree of incorporation of CLA isomers and dose-dependent reduction of arachidonic acid in total cell lipids of both types of vascular SMCs following treatment with CLA. The release of PGE₂ and PGI₂ was dose-dependently inhibited by either CLA isomer from both types of vascular SMCs. The inhibitory potential of CLA isomers on the release of prostanoids was slightly different between basal and cytokine-stimulated conditions. In conclusion, the present findings suggest that the action of CLA isomers on the release of vasoactive prostanoids from vascular SMCs is largely independent of the vascular location; e.g., coronary arteries or systemic vasculature (aorta), but partially depends on the pathophysiological status of SMCs. The observed anti-inflammatory effect of CLAs may contribute to the anti-atherogenic actions of CLA.