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首页> 外文期刊>Cell metabolism >SUMOylation-dependent LRH-1/PROX1 interaction promotes atherosclerosis by decreasing hepatic reverse cholesterol transport
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SUMOylation-dependent LRH-1/PROX1 interaction promotes atherosclerosis by decreasing hepatic reverse cholesterol transport

机译：SUMOylation依赖的LRH-1 / PROX1相互作用通过减少肝脏反向胆固醇转运促进动脉粥样硬化

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Reverse cholesterol transport (RCT) is an antiatherogenic process in which excessive cholesterol from peripheral tissues is transported to the liver and finally excreted from the body via the bile. The nuclear receptor liver receptor homolog 1 (LRH-1) drives expression of genes regulating RCT, and its activity can be modified by different posttranslational modifications. Here, we show that atherosclerosis-prone mice carrying a mutation that abolishes SUMOylation of LRH-1 on K289R develop less aortic plaques than control littermates when exposed to a high-cholesterol diet. The mechanism underlying this atheroprotection involves an increase in RCT and its associated hepatic genes and is secondary to a compromised interaction of LRH-1 K289R with the corepressor prospero homeobox protein 1 (PROX1). Our study reveals that the SUMOylation status of a single nuclear receptor lysine residue can impact the development of a complex metabolic disease such as atherosclerosis.
机译：胆固醇逆向转运（RCT）是一种抗动脉粥样硬化过程，其中来自周围组织的过量胆固醇被转运到肝脏，最后通过胆汁从体内排出。核受体肝受体同源物1（LRH-1）驱动调节RCT的基因的表达，并且其活性可以通过不同的翻译后修饰来修饰。在这里，我们显示，当暴露于高胆固醇饮食时，携带突变消除K289R上LRH-1的SUMOylation的易患动脉粥样硬化的小鼠比对照同窝出生的小鼠形成更少的主动脉斑块。这种抗动脉粥样硬化保护的机制涉及RCT及其相关肝基因的增加，并且是LRH-1 K289R与共加压素prospero同源盒蛋白1（PROX1）相互作用受损的第二个原因。我们的研究表明，单个核受体赖氨酸残基的SUMOylation状态会影响复杂代谢疾病（如动脉粥样硬化）的发展。

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