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

Nicotine regulates basic fibroblastic growth factor and transforming growth factorβ1 production in endothelial cells
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DOI:
10.1006/bbrc.1999.0478
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发表时间:
1999-04-13
影响因子:
3.1
通讯作者:
Cavallaro, A
Cavallaro, A
中科院分区:
生物学4区
文献类型:
--
作者:
Cucina, A;Corvino, V;Cavallaro, A

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尼古丁是吸烟的一种成分,可通过产生生长因子诱导动脉粥样硬化。研究了尼古丁(从6 × 10 - 4到6 × 10 - 8 M)刺激牛主动脉内皮细胞(EC)产生和释放bFGF和TGF β 1的模式。评估EC活力和计数。通过抑制抗体结合试验和Western印迹分析确定无血清条件培养基中bFGF和TGF β 1的存在。同时测定了尼古丁对EC的促有丝分裂活性。应用聚合酶链反应(PCR)检测bFGF和TGF β 1的表达。尼古丁刺激后bFGF的释放量大于对照组,而TGF β 1的释放量则较低。在尼古丁浓度为6 × 10(-6)M时,我们注意到最大的促有丝分裂活性。加入抗bFGF单克隆抗体可降低尼古丁暴露EC对氚标记胸苷的摄取,但加入抗TGF β 1单克隆抗体无显著影响,尼古丁暴露EC中bFGF mRNA表达显著高于对照组,而TGF β 1 mRNA表达无改变。从这些数据中,我们得出结论,尼古丁调节bFGF的产生和释放以及TGF β 1的释放,并可能在动脉粥样硬化的发展和进展中起关键作用。(C)北京:科学出版社.
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.