Conjugated linoleic acid isomers inhibit platelet-derived growth factor-induced NF-kappaB transactivation and collagen formation in human vascular smooth muscle cells.

BACKGROUND: Atherosclerosis is characterized by extensive thickening of the arterial intima partially resulting from deposition of collagen by vascular smooth muscle cells (SMCs). Polyunsaturated fatty acids stimulate collagen formation through NF-kappaB activation. AIM OF THE STUDY: The present study aimed to explore the effect of conjugated linoleic acids (CLAs) which are known to inhibit NF-kappaB activation on collagen formation by SMCs.
METHODS: Vascular SMCs were cultured with 50 micromol/l of CLA isomers (c9t11-CLA, t10c12-CLA) or linoleic acid (LA) and analysed for collagen formation and NF-kappaB p50 transactivation.
RESULTS: Treatment with CLA isomers but not LA significantly reduced PDGF-stimulated [(3)H] proline incorporation into cell layer protein of SMCs without altering cell proliferation. Simultaneous treatment with the PPARgamma inhibitor T0070907 abrogated this effect. Treatment of SMCs with c9t11-CLA and t10c12-CLA significantly reduced PDGF-induced NF-kappaB p50 activation.
CONCLUSIONS: CLA isomers inhibit PDGF-stimulated collagen production by vascular SMCs, which is considered to be a hallmark of atherosclerosis, in a PPARgamma-dependent manner. Whether inhibition of the NF-kappaB-pathway is of significance for the reduction of collagen formation by CLA isomers needs further investigation.