高密度脂蛋白抑制固醇调节元件结合蛋白-1 在培养细胞中的激活。
High density lipoprotein inhibits the activation of sterol regulatory element-binding protein-1 in cultured cells.
机构信息
Department of Nutrition and Metabolism, Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima-city, Japan.
出版信息
FEBS Lett. 2010 Mar 19;584(6):1217-22. doi: 10.1016/j.febslet.2010.02.034. Epub 2010 Feb 18.
A link between cellular uptake of high density lipoprotein (HDL) and regulation of sterol regulatory element-binding protein-1 (SREBP-1) was investigated in vitro. HDL decreased nuclear SREBP-1 levels as well as SREBP-1 target gene expression in HepG2 and HEK293 cells. However, HDL did not repress an exogenously expressed, constitutively active form of SREBP-1. HDL increased cellular cholesterol levels, and cellular cholesterol depletion by methyl-beta-cyclodextrin abolished the effects of HDL. These results suggest that HDL inhibits the activation of SREBP-1 through a cholesterol-dependent mechanism, which may play an important role in regulating lipid synthetic pathways mediated by SREBP-1.
在体外研究了细胞摄取高密度脂蛋白（HDL）与固醇调节元件结合蛋白-1（SREBP-1）调节之间的联系。HDL 降低了 HepG2 和 HEK293 细胞中的核 SREBP-1 水平以及 SREBP-1 靶基因的表达。然而，HDL 并没有抑制外源性表达的组成型激活形式的 SREBP-1。HDL 增加了细胞内胆固醇水平，而甲基-β-环糊精引起的细胞内胆固醇耗竭则消除了 HDL 的作用。这些结果表明，HDL 通过胆固醇依赖性机制抑制 SREBP-1 的激活，这可能在调节 SREBP-1 介导的脂质合成途径中发挥重要作用。
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