Marine Biotechnology Research Center Korea Institute of Ocean Science and Technology Busan Korea.
Department of Marine Biotechnology Korea University of Science and Technology Daejeon Korea.
FEBS Open Bio. 2019 Mar 12;9(4):769-780. doi: 10.1002/2211-5463.12619. eCollection 2019 Apr.
Fibroblast growth factor 11 (FGF11) is a member of the intracellular fibroblast growth factor superfamily. Here, we identified FGF11 as a novel mediator of adipogenesis. During 3T3-L1 adipocyte differentiation, the expression of FGF11 decreased at the mitotic clonal expansion stage and increased at the terminal differentiation stage. FGF11 knockdown reduced the expression of peroxisome proliferator-activated receptor gamma (PPARγ), a master regulator of adipogenesis, resulting in the inhibition of adipocyte differentiation. Treatment with the PPARγ agonist rosiglitazone restored the inhibition of adipogenesis caused by FGF11 knockdown. We also report that the expression of the PPARγ regulators CCAAT/enhancer-binding protein α, sterol regulatory element-binding protein 1, KLF9, KLF2, GATA binding factor 2, and GATA binding factor 3 was influenced by FGF11. These results suggest that FGF11 indirectly controls the expression of PPARγ through modifying the expression of multiple PPARγ regulators, thereby mediating adipogenesis.
成纤维细胞生长因子 11(FGF11)是细胞内成纤维细胞生长因子超家族的一员。在这里,我们鉴定出 FGF11 是脂肪生成的一个新的介质。在 3T3-L1 脂肪细胞分化过程中,FGF11 的表达在有丝分裂克隆扩增阶段下降,在终末分化阶段增加。FGF11 敲低降低了过氧化物酶体增殖物激活受体γ(PPARγ)的表达,PPARγ 是脂肪生成的主调控因子,导致脂肪细胞分化受到抑制。用 PPARγ 激动剂罗格列酮处理可恢复 FGF11 敲低引起的脂肪生成抑制。我们还报告说,PPARγ 调节因子 CCAAT/增强子结合蛋白α、固醇调节元件结合蛋白 1、KLF9、KLF2、GATA 结合因子 2 和 GATA 结合因子 3 的表达受 FGF11 影响。这些结果表明,FGF11 通过修饰多个 PPARγ 调节因子的表达,间接控制 PPARγ 的表达,从而介导脂肪生成。