Nicotine regulates basic fibroblastic growth factor and transforming growth factorβ1 production in endothelial cells

Nicotine, a constituent of cigarette smoking, may induce atherosclerosis through 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 and count were assessed. The presence of bFGF and TGF beta(1) in serum-free conditioned media was determined by the inhibition antibody-binding assay and Western blot analysis. Mitogenic activity of nicotine on EC was also determined. Polymerase chain reaction (PCR) was used to study the expression of bFGF and TGF beta(1). The bFGF release after nicotine stimulation was greater than controls, whereas TGF beta(1) release was lower. At a nicotine concentration of 6 x 10(-6) M we noted the greatest mitogenic activity. The addition of monoclonal antibody anti-bFGF decreased the tritiated thymidine uptake of EC exposed to nicotine but the addition of monoclonal antibody anti-TGF beta(1) had no significant effect, bFGF mRNA expression was significantly higher in EC exposed to nicotine than in controls, whereas TGF beta(1) mRNA expression was not modified. From these data we concluded that nicotine regulates bFGF production and release and TGF beta(1) release and may have a key role in the development and progression of atherosclerosis. (C) 1999 Academic Press.