Regulation of the expression of the avian uncoupling protein 3 by isoproterenol and fatty acids in chick myoblasts: possible involvement of AMPK and PPARα?
Regulation of the expression of the avian uncoupling protein 3 by isoproterenol and fatty acids in chick myoblasts: possible involvement of AMPK and PPARα?
复制标题
DOI：
10.1152/ajpregu.00087.2010
复制
发表时间：
2011-07-01
影响因子：
2.8
通讯作者：
Collin, Anne
中科院分区：
文献类型：
--
作者：
Joubert, Romain;Metayer-Coustard, Sonia;Collin, Anne
Joubert R，Metayer-Coustard S，Crochet S，Cailleau-Audouin E，Dupont J，Duclos MJ，Tesseraud S，柯林A.鸡成肌细胞中异丙肾上腺素和脂肪酸对禽类解偶联蛋白3表达的调节：AMPK和PPAR α的可能参与？Am J Physiol Regul Integr Comp Physiol 301：R201-R208，2011.首次发表于2011年4月20日; doi：10.1152/ajpregu.00087.2010.-鸟解偶联蛋白3（UCP 3）主要在肌肉组织中表达，可能参与脂肪酸代谢、限制活性氧产生和/或非颤抖性产热。我们最近证明，UCP 3 mRNA的表达增加异丙肾上腺素（ISO），β-激动剂，在鸡胸大肌。这种上调与FA代谢的变化以及AMP活化蛋白激酶（AMPK）活化和转录因子过氧化物酶体增殖物活化受体（PPAR）α、PPAR β/δ和PPAR γ共激活因子-1 α（PGC-1 α）表达的变化相关。本研究的目的是阐明AMPK和PPARalpha在鸡成肌细胞原代培养中UCP 3调控中的作用机制。与p38丝裂原活化蛋白激酶（p38 MAPK）激活相关的禽UCP 3 mRNA表达被Iso和/或FA增加。PKA通路介导Iso对UCP 3表达的影响。FA刺激也导致AMPK激活。此外，通过使用5-氨基咪唑-4-羧酰胺核糖核苷和化合物C显示AMPK对UCP 3调节的直接参与。使用与AMPK活化相关的p38 MAPK抑制剂SB 202190也显著增强UCP 3 mRNA表达。最后，PPAR α激动剂WY-14643强烈增加UCP 3 mRNA表达。这项研究强调了鸡成肌细胞中β-肾上腺素能系统和FA对UCP 3表达的控制，并证明其表达直接受AMPK和PPAR α调节。过表达的禽UCP 3可能调节能量利用或限制氧化应激时，线粒体代谢的FA被触发的儿茶酚胺。
Joubert R, Metayer-Coustard S, Crochet S, Cailleau-Audouin E, Dupont J, Duclos MJ, Tesseraud S, Collin A. Regulation of the expression of the avian uncoupling protein 3 by isoproterenol and fatty acids in chick myoblasts: possible involvement of AMPK and PPAR alpha? Am J Physiol Regul Integr Comp Physiol 301: R201-R208, 2011. First published April 20, 2011; doi:10.1152/ajpregu.00087.2010.-The avian uncoupling protein 3 (UCP3), mainly expressed in muscle tissue, could be involved in fatty acid (FA) metabolism, limitation of reactive oxygen species production, and/or nonshivering thermogenesis. We recently demonstrated that UCP3 mRNA expression was increased by isoproterenol (Iso), a beta-agonist, in chicken Pectoralis major. This upregulation was associated with changes in FA metabolism and variations in the activation of AMP-activated protein kinase (AMPK) and in the expression of the transcription factors peroxisome proliferator-activated receptor (PPAR)alpha, PPAR beta/delta, and PPAR gamma coactivator-1 alpha (PGC-1 alpha). The aim of the present study was to elucidate the mechanisms involving AMPK and PPAR alpha in UCP3 regulation in primary cultures of chick myoblasts. Avian UCP3 mRNA expression, associated with p38 mitogen-activated protein kinase (p38 MAPK) activation, was increased by Iso and/or FAs. The PKA pathway mediated the effects of Iso on UCP3 expression. FA stimulation also led to AMPK activation. Furthermore, the direct involvement of AMPK on UCP3 regulation was shown by using 5-aminoimidazole-4-carboxyamide ribonucleoside and Compound C. The use of the p38 MAPK inhibitor SB202190, which was associated with AMPK activation, also dramatically enhanced UCP3 mRNA expression. Finally the PPAR alpha agonist WY-14643 strongly increased UCP3 mRNA expression. This study highlights the control of UCP3 expression by the beta-adrenergic system and FA in chick myoblasts and demonstrates that its expression is directly regulated by AMPK and by PPAR alpha. Overexpression of avian UCP3 might modulate energy utilization or limit oxidative stress when mitochondrial metabolism of FA is triggered by catecholamines.