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首页> 外文期刊>Journal of Cellular Physiology >Excess Nitric Oxide Impairs LXR(alpha)-ABCA1 -Dependent Cholesterol Efflux in Macrophage Foam Cells
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Excess Nitric Oxide Impairs LXR(alpha)-ABCA1 -Dependent Cholesterol Efflux in Macrophage Foam Cells

机译：一氧化氮过剩损害LXR -ABCA1(α)端依赖在巨噬细胞胆固醇流出泡沫细胞

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Excess nitric oxide (NO) promotes the progression of atherosclerosis by increasing the oxidation of low-density lipoprotein (LDL) and inflammatory responses. However, little is known about the impact of NO and its underlying molecular mechanism on lipid metabolism of macrophage foam celis. in this study, Oil-red O staining, cholesterol and triglyceride assay, Oil-oxidized LDL (oxLDL) binding assay, cholesterol efflux assay, real-time RT-PCR and Western blot analysis were used for in vitro experiments. Apolipoprotein E-deficient (apoE~(-/-)) and apoE and inducible nitric oxide synthase-deficient (apoE~(-/-)iNGS~(-/-)) mice were as our in vivo models. Treatment with S-nitroso-N-acetyi-D,L-penicillamine (SNAP), an NO donor, exacerbated oxLDL-induced cholesterol accumulation in macrophages, because of reduced efficacy of cholesterol efflux. In addition, SNAP decreased the protein level of ATP-binding cassette transporter AI (ABCAi) without affecting scavenger receptor type A (SR-A), CD36, ABCGI, or SR-BI levels. This SNAP-mediated downregulation of ABCAI was mainly through the effect of NO but not peroxynitrite. Furthermore, the SNAP-downregulated ABCAI was due to the decrease in the liver X receptor alpha (LXRalpha)-dependent transcriptional regulation. Moreover, genetic deletion of iNOS increased the serum capacity of reverse cholesteroi efflux and protein expression of LXRalpha, ABCAI, and SR-BS in aortas and retarded atherosclerosis in apoE~(-/-) mice. Our findings provide new insights in the pro-atherogenic effect of excess NO on cholesterol metabolism in macrophages.
机译：多余的一氧化氮(NO)促进发展动脉粥样硬化的增加的氧化低密度脂蛋白(LDL)和炎症响应。不影响及其潜在的分子机制对脂质代谢的巨噬细胞泡沫附加评论。胆固醇和甘油三酯测定,Oil-oxidized低密度脂蛋白(oxLDL)绑定化验,胆固醇流出分析、实时rt - pcr和免疫印迹分析被用于体外实验。载脂蛋白E-deficient (apoE ~(- / -))和载脂蛋白e和诱导一氧化氮synthase-deficient(apoE ~(- / -)寄托~(- / -)小鼠体内模型。S-nitroso-N-acetyi-D L-penicillamine(吸附)没有捐赠,加剧了oxLDL-induced胆固醇的巨噬细胞中积累,因为减少了胆固醇流出的效果。蛋白的磷酸腺苷水平下降盒式运输车AI (ABCAi)而不影响清道夫受体A型(SR-A), CD36 ABCGI或SR-BI水平。ABCAI主要是通过没有但是的效果过氧亚硝基。SNAP-downregulated ABCAI是由于减少在肝X受体α(LXRalpha)端依赖转录监管。此外,基因删除伊诺增加了血清的能力扭转cholesteroi流出蛋白质表达LXRalpha ABCAI, SR-BS在主动脉和迟钝的动脉粥样硬化载脂蛋白e ~(- / -)小鼠。见解pro-atherogenic过剩的影响没有在巨噬细胞胆固醇代谢。

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