Upregulation of Fas and FasL expression in nicotine-induced apoptosis of endothelial cells

Abstract

Although smoking-related coronary vascular disease is well documented, the effects of nicotine have not been fully investigated. There is controversy over reports about the effect of nicotine on apoptosis. The effect of nicotine on apoptosis of human umbilical vein endothelial cells (HUVECs) and the expressions of Fas/Fas ligand (FasL) and caspase-3 were evaluated in this study. Annexin V fluorescein isothiocyanate and propidium iodide double staining demonstrated that nicotine (0.2 microM, 0.5 microM and 1 microM) could induce apoptosis of HUVECs; reverse transcription (RT)-PCR and Western blotting analysis demonstrated that levels of Fas and FasL expression were increased in nicotine-treated HUVECs. Moreover, caspase-3 expression was also increased. These data indicate that nicotine induces the apoptosis of HUVECs, and that the Fas/FasL pathway may play an important role. This provides evidence that nicotine may have an important role in cardiovascular pathology and atherogenesis.

Smoking and Rheumatoid Arthritis

“…Smoking can both increase and decrease apoptosis, depending on the cell types [ 23 , 24 ]. It was reported that smoking increases the levels of Fas (CD95) and CD4 T-cells that make cells more vulnerable to apoptosis, leading to high levels of cellular debris, which may not be adequately cleared in autoimmune diseases [ 23 ].…”

“…Smoking can both increase and decrease apoptosis, depending on the cell types [ 23 , 24 ]. It was reported that smoking increases the levels of Fas (CD95) and CD4 T-cells that make cells more vulnerable to apoptosis, leading to high levels of cellular debris, which may not be adequately cleared in autoimmune diseases [ 23 ]. Bijl et al reported that smoking was associated with an increase in the percentage of Fas-expressing CD4+ T and B lymphocytes; however, there were no differences between smokers and non-smokers in in vitro Fas-induced apoptosis and the percentages of circulating apoptotic lymphocytes between smokers and non-smokers [ 24 ].…”

“…Bijl et al reported that smoking was associated with an increase in the percentage of Fas-expressing CD4+ T and B lymphocytes; however, there were no differences between smokers and non-smokers in in vitro Fas-induced apoptosis and the percentages of circulating apoptotic lymphocytes between smokers and non-smokers [ 24 ]. Cheng et al demonstrated that nicotine induced the apoptosis of human umbilical vein endothelial cells by the Fas/FasL pathway [ 23 ]. However, Imirzalioĝlu et al showed that the mean soluble Fas levels were significantly lower in the saliva of smokers’ than in that of non-smokers’, suggesting smoking might induce anti-apoptotic mechanisms in the oral cavity [ 25 ].…”

Association between secondhand smoke exposure and rheumatoid arthritis in US never-smoking adults: a cross-sectional study from NHANES

“…Last but not least, smoking elevates the levels of Fas (CD95) and CD4 T-cells, making cells more prone to apoptosis. This heightened susceptibility to apoptosis results in increased levels of cellular debris, which might not be sufficiently eliminated in autoimmune disorders 37 . Smoking influences the immune system, resulting in diminished natural killer cells, suppressed hormonal cells, and cell-mediated immunity, along with the induction of dysfunction in T lymphocytes [38][39][40][41][42] .…”