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 micromol/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-alpha (TNFalpha) (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.
Ringseis
Robert
R
Institut für Ernährungswissenschaften, Martin-Luther-Universität Halle-Wittenberg, D-06108 Halle/Saale, Germany. robert.ringseis@landw.uni-halle.de
Gahler
Susan
S
Herter
Christian
C
Eder
Klaus
K
D001011:Aorta; D003331:Coronary Vessels; D051546:Cyclooxygenase 2 / Q000378:metabolism; D015232:Dinoprostone / Q000037:antagonists & inhibitors / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D011464:Epoprostenol / Q000037:antagonists & inhibitors / Q000378:metabolism*; D006801:Humans; D007536:Isomerism; D044243:Linoleic Acids, Conjugated / Q000494:pharmacology*; D050356:Lipid Metabolism / Q000187:drug effects; D032389:Myocytes, Smooth Muscle / Q000187:drug effects* / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D044243:Linoleic Acids, Conjugated; D014409:Tumor Necrosis Factor-alpha; C503589:cis-9, trans-11-conjugated linoleic acid; D011464:Epoprostenol; D051546:Cyclooxygenase 2; D015232:Dinoprostone