Microarray evaluation of EP4 receptor-mediated prostaglandin E2 suppression of 3T3-L1 adipocyte differentiation.
Microarray evaluation of EP4 receptor-mediated prostaglandin E2 suppression of 3T3-L1 adipocyte differentiation.
复制标题
DOI：
10.1016/j.bbrc.2004.07.194
复制
发表时间：
2004-09
影响因子：
3.1
通讯作者：
Y. Sugimoto;Hiroaki Tsuboi;Y. Okuno;Shigero Tamba;Soken Tsuchiya;G. Tsujimoto;A. Ichikawa
中科院分区：
文献类型：
--
作者：
Y. Sugimoto;Hiroaki Tsuboi;Y. Okuno;Shigero Tamba;Soken Tsuchiya;G. Tsujimoto;A. Ichikawa
前列腺素E2（PGE 2）已被证明负调节脂肪形成。为了探索PGE 2在多大程度上抑制细胞向脂肪细胞的分化，并检查其作用是否可能是由于EP 4受体信号传导，我们使用微阵列分析暴露于补充有PGE 2、AE 1 -329（EP 4激动剂）或载体的分化鸡尾酒的3 T3-L1细胞的基因表达谱。PGE 2处理后，脂肪细胞因子和脂代谢相关酶等基因的分化相关反应大大减弱。特别是，过氧化物酶体增殖物激活受体-γ和CCAAT/增强子结合蛋白-α的表达，在脂肪形成中发挥核心作用的基因，大大抑制。PGE 2对己糖激酶2和磷酸果糖激酶等胰岛素靶基因亚类无效。AE 1 -329处理后，分化相关基因中产生了类似的反应。这些结果表明，PGE 2通过作用于3 T3-L1细胞中的EP 4受体来抑制脂肪细胞分化过程中的关键步骤。
Prostaglandin E2(PGE2) has been shown to negatively regulate adipogenesis. To explore to what extent PGE2inhibits the differentiation of cells to adipocytes and to examine whether its effect could be due to EP4 receptor signaling, we used microarrays to analyze the gene expression profiles of 3T3-L1 cells exposed to a differentiation cocktail supplemented with PGE2, AE1-329 (an EP4 agonist), or vehicle. The differentiation-associated responses in genes such as adipocytokines and enzymes related to lipid metabolism were largely weakened upon PGE2treatment. In particular, the expression of peroxisome proliferator activated receptor-γ and CCAAT/enhancer binding protein-α, genes playing a central role in adipogenesis, was greatly suppressed. PGE2appears to be ineffective to a subclass of insulin target genes such as hexokinase 2 and phosphofructokinase. Similar responses were produced in the differentiation-associated genes upon AE1-329 treatment. These results suggest that PGE2inhibits a crucial step of the adipocyte differentiation process by acting on the EP4 receptor in 3T3-L1 cells.