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内皮素-1抑制脂肪生成:Akt和ERK1/2磷酸化的作用

Endothelin-1 inhibits adipogenesis: role of phosphorylation of Akt and ERK1/2.

作者信息

Bhattacharya Indranil, Ullrich Axel

机构信息

Department of Molecular Biology, Max Planck Institute for Biochemistry, Am Klopferspitz 18, D-82152 Martinsried, Germany.

出版信息

FEBS Lett. 2006 Oct 16;580(24):5765-71. doi: 10.1016/j.febslet.2006.09.032. Epub 2006 Sep 27.

DOI:10.1016/j.febslet.2006.09.032
PMID:17022980
Abstract

In adipogenesis, growth factors play a crucial role. Using serum depleted condition, we studied the causal role of endothelin-1 (ET-1) and epidermal growth factor (EGF), separately or together, in adipocyte differentiation of 3T3-L1 cells. ET-1 stimulation caused an anti-adipogenic response and this effect was potentiated upon treatment with EGF. Co-treatment with EGF and ET-1 blocked the expression of C/EBPalpha and PPARgamma, the adipogenic markers. The inhibition of adipogenesis was preceded by a biphasic (early and late) attenuation of Akt phosphorylation. We suggest that treatment with ET-1 and EGF together induce a more potent anti-adipogenic response, involving increased Erk1/2 phosphorylation and biphasic attenuation of Akt phosphorylation.

摘要

在脂肪生成过程中,生长因子起着至关重要的作用。利用血清缺乏条件,我们分别或共同研究了内皮素-1(ET-1)和表皮生长因子(EGF)在3T3-L1细胞脂肪分化中的因果作用。ET-1刺激引起抗脂肪生成反应,且在用EGF处理后这种效应增强。EGF和ET-1共同处理可阻断脂肪生成标志物C/EBPα和PPARγ的表达。脂肪生成的抑制之前是Akt磷酸化的双相(早期和晚期)减弱。我们认为,ET-1和EGF共同处理可诱导更强的抗脂肪生成反应,这涉及Erk1/2磷酸化增加和Akt磷酸化的双相减弱。

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