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肝脏特异性的Lxr抑制抑制胆固醇养小鼠的逆胆固醇运输

Takafumi Nishida¹, Makoto Ayaori², Junko Arakawa¹

¹Division of Anti-aging and Vascular Medicine, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan.

Atherosclerosis

|May 26, 2024

概括

肝硫转移酶家族细胞质2B成员1 (Sult2b1) 的过度表达通过减少肝X受体 (Lxr) 向基因表达来抑制高密度脂蛋白 (HDL) 水平和逆胆固醇输送 (RCT). 这些效应是依赖Lxr的.

科学领域:

心血管生物学心血管生物学
脂质代谢脂质代谢是什么
分子内分泌学分子内分泌学

背景情况:

高密度脂蛋白 (HDL) 在逆胆固醇运输 (RCT) 中起着至关重要的作用,这是一个抗动脉样硬化过程.
肝X受体 (Lxrs) 是RCT的关键转录调节器,但肝X受体在体内Lxrs的作用尚不清楚.

研究的目的:

研究肝脏Lxr抑制对小鼠的HDL水平和RCT的影响.
阐明肝硫转移酶家族细胞质2B成员1 (Sult2b1) 在调节Lxr依赖路径中的作用.

主要方法:

在野生型和Lxrα/β双淘汰赛小鼠中,腺病毒载体介导的Sult2b1 (Ad-Sult2b1) 过度表达.
维持小鼠在正常或高胆固醇饮食.
进行了巨细胞RCT测定和HDL动力学研究.

主要成果:

肝脏Sult2b1过度表达减少了Lxr目标基因表达,导致HDL胆固醇降低和阿波利波蛋白B-脂蛋白 (apoB-L) 水平增加.
在高胆固醇饮食下,Sult2b1抑制了巨细胞衍生胆固醇的便分泌.
通过Ad-Sult2b1促进高密度胆固醇 (HDL) 代谢和肝脏吸收,从而减少便的分泌.
在Lxr缺乏的小鼠中,Sult2b1增加了apoB-L,但没有影响HDL水平或RCT,表明HDL/RCT的Lxr依赖调节.

结论:

肝脏Lxr抑制对循环中的HDL水平和RCT产生负面调节.
减少Lxr目标基因表达是这些影响背后的机制.
通过Sult2b1调节的HDL/RCT与其对apoB-L的影响不同,并且依赖于Lxr.

关键词:

携带ATP绑定磁带的传送器G5/G8 胆固醇7α氧化酶的使用这就是HDL胆固醇.硫转移酶家族的细胞质2B成员1 (Sult2b1)

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