Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, United States of America.
PLoS One. 2012;7(8):e42915. doi: 10.1371/journal.pone.0042915. Epub 2012 Aug 17.
The disruption of cholesterol homeostasis leads to an increase in cholesterol levels which results in the development of cardiovascular disease. Mitogen Inducible Gene 6 (Mig-6) is an immediate early response gene that can be induced by various mitogens, stresses, and hormones. To identify the metabolic role of Mig-6 in the liver, we conditionally ablated Mig-6 in the liver using the Albumin-Cre mouse model (Alb(cre/+)Mig-6(f/f); Mig-6(d/d)). Mig-6(d/d) mice exhibit hepatomegaly and fatty liver. Serum levels of total, LDL, and HDL cholesterol and hepatic lipid were significantly increased in the Mig-6(d/d) mice. The daily excretion of fecal bile acids was significantly decreased in the Mig-6(d/d) mice. DNA microarray analysis of mRNA isolated from the livers of these mice showed alterations in genes that regulate lipid metabolism, bile acid, and cholesterol synthesis, while the expression of genes that regulate biliary excretion of bile acid and triglyceride synthesis showed no difference in the Mig-6(d/d) mice compared to Mig-6(f/f) controls. These results indicate that Mig-6 plays an important role in cholesterol homeostasis and bile acid synthesis. Mice with liver specific conditional ablation of Mig-6 develop hepatomegaly and increased intrahepatic lipid and provide a novel model system to investigate the genetic and molecular events involved in the regulation of cholesterol homeostasis and bile acid synthesis. Defining the molecular mechanisms by which Mig-6 regulates cholesterol homeostasis will provide new insights into the development of more effective ways for the treatment and prevention of cardiovascular disease.
胆固醇稳态的破坏会导致胆固醇水平升高,从而导致心血管疾病的发生。有丝分裂原诱导基因 6(Mig-6)是一种即刻早期反应基因,可被各种有丝分裂原、应激和激素诱导。为了确定 Mig-6 在肝脏中的代谢作用,我们使用白蛋白-Cre 小鼠模型(Alb(cre/+)Mig-6(f/f);Mig-6(d/d))条件性地在肝脏中敲除了 Mig-6。Mig-6(d/d) 小鼠表现出肝肿大和脂肪肝。Mig-6(d/d) 小鼠的血清总胆固醇、LDL 胆固醇和 HDL 胆固醇及肝脂质水平显著升高。Mig-6(d/d) 小鼠粪便胆汁酸的日排泄量显著减少。对这些小鼠肝脏中分离的 mRNA 进行 DNA 微阵列分析显示,调节脂质代谢、胆汁酸和胆固醇合成的基因发生了改变,而调节胆汁酸和甘油三酯合成的胆汁酸胆道排泄的基因表达在 Mig-6(d/d) 小鼠与 Mig-6(f/f) 对照之间没有差异。这些结果表明 Mig-6 在胆固醇稳态和胆汁酸合成中发挥重要作用。肝脏特异性敲除 Mig-6 的小鼠会发生肝肿大和肝内脂质增加,并提供了一个新的模型系统来研究调节胆固醇稳态和胆汁酸合成的遗传和分子事件。确定 Mig-6 调节胆固醇稳态的分子机制将为开发更有效的心血管疾病治疗和预防方法提供新的见解。