Hirai Shizuka, Yamanaka Mai, Kawachi Hiroyuki, Matsui Tohru, Yano Hideo
Division of Applied Biosciences, Graduate School of Agriculture, Kyoto University, Kitashirakawa-oiwake, Sakyo-ku, Kyoto-shi 606-8502, Japan.
Mol Cell Endocrinol. 2005 Mar 31;232(1-2):21-6. doi: 10.1016/j.mce.2005.01.001.
We investigated the effect of activin A on differentiation of 3T3-L1 preadipocyte. Activin A suppressed the induction of terminal differentiation markers such as glycerol-3-phosphate dehydrogenase (GPDH) activity, lipid accumulation, and the expression of adipocyte fatty acid-binding protein (aP2) mRNA when the cells were treated with activin A throughout the differentiation period. Activin A treatment during the early phase decreased GPDH activity and aP2 mRNA level, and also reduced the expression of peroxisome proliferator-activated receptor (PPAR) gamma and CCAAT/enhancer binding protein (C/EBP) alpha mRNAs without affecting the expressions of the active isoforms of C/EBPbeta and its mRNA. On the other hand, activin A treatment had no effect on the mitotic clonal expansion. These results indicate that activin A inhibits adipogenesis via affecting the transcriptional factor cascade upstream of PPARgamma expression.
我们研究了激活素A对3T3-L1前脂肪细胞分化的影响。当在整个分化期用激活素A处理细胞时,激活素A抑制了终末分化标志物的诱导,如甘油-3-磷酸脱氢酶(GPDH)活性、脂质积累以及脂肪细胞脂肪酸结合蛋白(aP2)mRNA的表达。在早期用激活素A处理可降低GPDH活性和aP2 mRNA水平,还可减少过氧化物酶体增殖物激活受体(PPAR)γ和CCAAT/增强子结合蛋白(C/EBP)α mRNA的表达,而不影响C/EBPβ活性异构体及其mRNA的表达。另一方面,激活素A处理对有丝分裂克隆扩增没有影响。这些结果表明,激活素A通过影响PPARγ表达上游的转录因子级联反应来抑制脂肪生成。