Sakamoto Kei, Hirshman Michael F, Aschenbach William G, Goodyear Laurie J
Research Division, Joslin Diabetes Center and the Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02215, USA.
J Biol Chem. 2002 Apr 5;277(14):11910-7. doi: 10.1074/jbc.M112410200. Epub 2002 Jan 23.
The protein serine/threonine kinase Akt/protein kinase B has been recognized as a critical signaling mediator for multiple cell systems. The function of Akt in skeletal muscle is not well understood, and whether contractile activity stimulates Akt activity has been controversial. In the current study, contraction in situ, induced via sciatic nerve stimulation, significantly increased Akt Ser(473) phosphorylation in multiple muscle types including the extensor digitorum longus (13-fold over basal), plantaris (5.8-fold), red gastrocnemius (4.7-fold), white gastrocnemius (3.3-fold), and soleus (1.6-fold). In addition to increasing phosphorylation, contraction in situ significantly increased the activity of all three Akt isoforms (Akt1 > Akt2 > Akt3) with maximal activation occurring at 2.5 min and returning to base line with 15 min of contraction. Akt phosphorylation and activity were also increased when isolated muscles were contracted in vitro in the absence of systemic factors, although to a much lesser extent. The phosphatidylinositol 3-kinase inhibitors wortmannin and LY294002 fully inhibited contraction-stimulated Akt phosphorylation and activity but did not diminish contraction-stimulated glycogen synthase kinase-3 phosphorylation and glycogen synthase activity. These results demonstrate that contraction increases Akt phosphorylation and activity in skeletal muscle and that this stimulation is rapid, transient, muscle fiber type-specific, and wortmannin- and LY294002-inhibitable. Akt signaling is not necessary for the regulation of glycogen synthase activity in contracting skeletal muscle.
蛋白质丝氨酸/苏氨酸激酶Akt/蛋白激酶B已被公认为多种细胞系统的关键信号转导介质。Akt在骨骼肌中的功能尚未完全了解,收缩活动是否会刺激Akt活性一直存在争议。在当前研究中,通过坐骨神经刺激诱导的原位收缩显著增加了多种肌肉类型中Akt Ser(473)的磷酸化,包括趾长伸肌(比基础水平高13倍)、跖肌(5.8倍)、红色腓肠肌(4.7倍)、白色腓肠肌(3.3倍)和比目鱼肌(1.6倍)。除了增加磷酸化外,原位收缩还显著增加了所有三种Akt亚型(Akt1 > Akt2 > Akt3)的活性,最大激活发生在2.5分钟,收缩15分钟后恢复到基线水平。在没有全身因素的情况下,体外收缩分离的肌肉时,Akt的磷酸化和活性也会增加,尽管程度要小得多。磷脂酰肌醇3-激酶抑制剂渥曼青霉素和LY294002完全抑制收缩刺激的Akt磷酸化和活性,但不会降低收缩刺激的糖原合酶激酶-3磷酸化和糖原合酶活性。这些结果表明,收缩会增加骨骼肌中Akt的磷酸化和活性,并且这种刺激是快速、短暂、肌肉纤维类型特异性的,并且可被渥曼青霉素和LY294002抑制。Akt信号传导对于收缩骨骼肌中糖原合酶活性的调节不是必需的。