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首页> 外文期刊>The Journal of Nutritional Biochemistry >Unsaturated fatty acids repress expression of ATP binding cassette transporter A1 and G1 in RAW 264.7 macrophages
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Unsaturated fatty acids repress expression of ATP binding cassette transporter A1 and G1 in RAW 264.7 macrophages

机译：不饱和脂肪酸抑制RAW 264.7巨噬细胞中ATP结合盒转运蛋白A1和G1的表达

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摘要

Reverse cholesterol transport (RCT), a process to deliver excess cholesterol from the periphery to the liver for excretion from body, is a major atheroprotective property of high-density lipoproteins. As major transporters for cholesterol efflux in macrophages, ATP-binding cassette transporter A1 (ABCA1) and G1 (ABCG1) are critical for RCT. We investigated mechanisms for the regulation of ABCA1 and ABCG1 expression by fatty acids (FA) in RAW264.7 macrophages. Cells were incubated with 100 micro mol/L of palmitic, oleic, linoleic, linolenic or eicosapentaenoic acids in the absence or presence of T0901317, a liver X receptor (LXR) agonist. Unsaturated FA, but not saturated FA, significantly reduced ABCA1 and ABCG1 mRNA without the agonist. Trichostatin A (TSA), a histone deacetylase inhibitor, not only increased basal ABC transporter expression but abrogated the transcriptional repression by unsaturated FA. The increased basal ABCA1 and ABCG1 mRNA by TSA paralleled the increased peroxisome proliferator-activated receptor gamma (PPAR gamma ) and PPAR gamma coactivator 1 alpha expression, whereas LXR alpha and PGC-1 beta expression was significantly lowered. Although the repressive effect of ABCA1 and ABCG1 mRNA by unsaturated FA was abolished by T0901317, protein levels remained diminished. Chemical and genetic deficiency of protein kinase C delta did not abolish the repressive effect of linoleic acid on ABCA1 and ABCG1. In conclusion, unsaturated FA repressed ABCA1 and ABCG1 expression by two distinct mechanisms in RAW 264.7 macrophages: LXR-dependent transcriptional repression possibly by modulating histone acetylation state and LXR-independent posttranslational inhibition.
机译：反向胆固醇运输（RCT）是一种将多余的胆固醇从外周输送到肝脏以从体内排泄的过程，是高密度脂蛋白的主要抗动脉粥样硬化特性。作为巨噬细胞胆固醇外流的主要转运蛋白，ATP结合盒转运蛋白A1（ABCA1）和G1（ABCG1）对于RCT至关重要。我们调查了RAW264.7巨噬细胞中脂肪酸（FA）调节ABCA1和ABCG1表达的机制。在不存在或存在肝X受体（LXR）激动剂T0901317的情况下，将细胞与100微摩尔/升的棕榈酸，油酸，亚油酸，亚麻酸或二十碳五烯酸一起孵育。不饱和FA，但不饱和FA，可显着降低没有激动剂的ABCA1和ABCG1 mRNA。组蛋白脱乙酰基酶抑制剂曲古他汀A（TSA）不仅增加了基础ABC转运蛋白的表达，而且废除了不饱和FA的转录抑制作用。 TSA增加的基础ABCA1和ABCG1 mRNA的表达与过氧化物酶体增殖物激活的受体伽玛（PPAR gamma）和PPAR伽玛共激活因子1α的表达平行，而LXRα和PGC-1β的表达显着降低。尽管T0901317消除了不饱和FA对ABCA1和ABCG1 mRNA的抑制作用，但蛋白质水平仍然降低。蛋白激酶Cδ的化学和遗传缺陷并未消除亚油酸对ABCA1和ABCG1的抑制作用。总之，不饱和脂肪酸通过两种不同的机制在RAW 264.7巨噬细胞中抑制ABCA1和ABCG1的表达：可能通过调节组蛋白乙酰化状态和LXR独立的翻译后抑制来抑制LXR依赖的转录。

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