Aouadi M, Jager J, Laurent K, Gonzalez T, Cormont M, Binétruy B, Le Marchand-Brustel Y, Tanti J-F, Bost F
INSERM, U 568, IFR50, F-06107, Nice, France.
FEBS Lett. 2007 Dec 11;581(29):5591-6. doi: 10.1016/j.febslet.2007.10.064. Epub 2007 Nov 13.
Little is known about the role of p38MAPK in human adipocyte differentiation. Here we showed that p38MAPK activity increases during human preadipocytes differentiation. Pharmacological inhibition of p38MAPK during adipocyte differentiation of primary human preadipocytes markedly reduced triglycerides accumulation and adipocyte markers expression. Cell cycle arrest or proliferation was not affected by p38MAPK inhibition. Although induction of C/EBPbeta was not altered by the p38MAPK inhibitor, its phosphorylation on Threonine(188) was decreased as well as PPARgamma expression. These results indicate that p38MAPK plays a positive role in human adipogenesis through regulation of C/EBPbeta and PPARgamma factors.
关于p38丝裂原活化蛋白激酶(p38MAPK)在人类脂肪细胞分化中的作用,人们所知甚少。在此我们表明,在人类前脂肪细胞分化过程中,p38MAPK活性增加。在原代人类前脂肪细胞的脂肪细胞分化过程中,对p38MAPK进行药理学抑制可显著减少甘油三酯积累和脂肪细胞标志物的表达。细胞周期停滞或增殖不受p38MAPK抑制的影响。虽然p38MAPK抑制剂未改变C/EBPβ的诱导,但苏氨酸(188)位点的磷酸化以及PPARγ表达均降低。这些结果表明,p38MAPK通过调节C/EBPβ和PPARγ因子在人类脂肪生成中发挥积极作用。