Department of Biological Sciences, College of Natural Sciences, Chonnam National University, Buk-Gu, Gwangju, South Korea.
FEBS Lett. 2011 Sep 2;585(17):2763-7. doi: 10.1016/j.febslet.2011.08.002. Epub 2011 Aug 11.
We show that TR4 facilitates lipid accumulation in 3T3-L1 adipocytes via induction of the FATP1 gene. Further study showed that TR4 transactivated FATP1 5' promoter activity via direct binding to the TR4 responsive element located at the FATP1 5' promoter region. Constitutive overexpression of TR4 in 3T3-L1 adipocytes resulted in increased lipid accumulation, accompanied by an increase in fatty acid uptake. However, small interfering RNA knockdown of FATP1 abolished TR4-enhanced fatty acid uptake. Moreover, microRNA-mediated silencing of TR4 in 3T3-L1 adipocytes drastically reduced basal FATP1 5' promoter activity and FATP1 expression with reduced lipid accumulation.
我们证明 TR4 通过诱导 FATP1 基因促进 3T3-L1 脂肪细胞中的脂质积累。进一步的研究表明，TR4 通过直接结合位于 FATP1 5'启动子区域的 TR4 反应元件来转激活 FATP1 5'启动子活性。TR4 在 3T3-L1 脂肪细胞中的组成性过表达导致脂质积累增加，伴随着脂肪酸摄取的增加。然而，FATP1 的小干扰 RNA 敲低消除了 TR4 增强的脂肪酸摄取。此外，在 3T3-L1 脂肪细胞中用 microRNA 介导的 TR4 沉默极大地降低了基础 FATP1 5'启动子活性和 FATP1 表达，伴随着脂质积累的减少。
