Skeletal muscle contractile activity in vitro stimulates mitogen-activated protein kinase signaling.

Skeletal muscle contractile activity in vitro stimulates mitogen-activated protein kinase signaling.
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体外骨骼肌收缩活动刺激有丝分裂原激活的蛋白激酶信号传导。

DOI:
10.1152/ajpcell.1999.277.4.c701
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发表时间:
1999
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Goodyear,LJ
Goodyear,LJ
中科院分区:
--
文献类型:
--
作者:
Hayashi,T;Hirshman,MF;Dufresne,SD;Goodyear,LJ

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体育锻炼是丝裂原活化蛋白(MAP)激酶信号传导的有效刺激剂。为了确定这种激活是否继发于对运动的全身反应或由于肌肉收缩活动本身,开发了分离的肌肉制备物。在体外收缩活动显着增加p44 MAPK和p42 MAPK磷酸化的2.9和2.4倍,分别。收缩刺激的MAP激酶磷酸化没有减少的存在ofd-筒箭毒碱或calphostin C,这表明既不释放神经递质,也不二酰基甘油敏感的蛋白激酶C介导的收缩诱导激活的信号级联反应。然而,PD-98059,MAP激酶激酶(MEK)的抑制剂,抑制收缩诱导的MAP激酶磷酸化的增加。PD-98059未改变收缩诱导的葡萄糖摄取或糖原合酶活性增加,表明MAP激酶信号传导对于骨骼肌收缩活性的这些重要代谢效应并非必需。这些数据表明,骨骼肌纤维本身的收缩活动,而不是对神经递质释放,激素或其他全身因素的反应,是负责刺激MAP激酶信号与体育锻炼。
Physical exercise is a potent stimulator of mitogen-activated protein (MAP) kinase signaling. To determine if this activation is secondary to systemic responses to exercise or due to muscle contractile activity per se, an isolated muscle preparation was developed. Contractile activity in vitro significantly increased p44MAPKand p42MAPKphosphorylation by 2.9- and 2.4-fold, respectively. Contraction-stimulated MAP kinase phosphorylation was not decreased in the presence ofd-tubocurarine or calphostin C, suggesting that neither neurotransmitter release nor diacylglycerol-sensitive protein kinase C mediates the contraction-induced activation of this signaling cascade. However, PD-98059, an inhibitor of MAP kinase kinase (MEK), inhibited the contraction-induced increases in MAP kinase phosphorylation. PD-98059 did not alter contraction-induced increases in glucose uptake or glycogen synthase activity, demonstrating that MAP kinase signaling is not necessary for these important metabolic effects of contractile activity in skeletal muscle. These data suggest that contractile activity of the skeletal muscle fibers per se, and not responses to neurotransmitter release, hormones, or other systemic factors, is responsible for the stimulation of MAP kinase signaling with physical exercise.
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