Nicotine regulates basic fibroblastic growth factor and transforming growth factor beta(1) production in endothelial cells

Nicotine, a constituent of cigarette smoking, may induce atherosclerosis th rough the production of growth factors. The pattern of bFGF and TGF beta(1) production and release by bovine aortic endothelial cells (EC) stimulated with nicotine (from 6 x 10(-4) to 6 x 10(-8) M) was studied. EC viability a nd count were assessed. The presence of bFGF and TGF beta(1) in serum-free conditioned media was determined by the inhibition antibody-binding assay a nd Western blot analysis. Mitogenic activity of nicotine on EC was also det ermined. Polymerase chain reaction (PCR) was used to study the expression o f bFGF and TGF beta(1). The bFGF release after nicotine stimulation was gre ater than controls, whereas TGF beta(1) release was lower. At a nicotine co ncentration of 6 x 10(-6) M we noted the greatest mitogenic activity. The a ddition of monoclonal antibody anti-bFGF decreased the tritiated thymidine uptake of EC exposed to nicotine but the addition of monoclonal antibody an ti-TGF beta(1) had no significant effect, bFGF mRNA expression was signific antly higher in EC exposed to nicotine than in controls, whereas TGF beta(1 ) mRNA expression was not modified. From these data we concluded that nicot ine regulates bFGF production and release and TGF beta(1) release and may h ave a key role in the development and progression of atherosclerosis. (C) 1 999 Academic Press.