Regulatory mechanisms of SNAT2, an amino acid transporter, in L6 rat skeletal muscle cells by insulin, osmotic shock and amino acid deprivation
Regulatory mechanisms of SNAT2, an amino acid transporter, in L6 rat skeletal muscle cells by insulin, osmotic shock and amino acid deprivation
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DOI：
10.1007/s00726-008-0050-9
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发表时间：
2009-02-01
期刊：
影响因子：
3.5
通讯作者：
Sugawara, Mitsuru
中科院分区：
文献类型：
--
作者：
Kashiwagi, Hitoshi;Yamazaki, Kojiro;Sugawara, Mitsuru
多项研究表明，胰岛素、渗透压休克和氨基酸剥夺可上调A系统的活性。然而，其机制尚不清楚。我们利用L6大鼠骨骼肌细胞进行研究，以阐明胰岛素、渗透压休克和氨基酸剥夺上调A系统活性的机制。这种上调是由于V(Max)的增加，而不是K(M)的增加。氯喹和Wortmannin可抑制胰岛素刺激和氨基酸剥夺引起的上调，但不能抑制渗透性休克引起的上调。而放线菌素D、放线菌素D和放线菌素D则可抑制上述两种刺激的上调。此外，PD98059和SP600125仅抑制氨基酸剥夺诱导的上调，SB202190仅抑制胰岛素诱导的上调。我们的研究结果表明，胰岛素、渗透压休克和氨基酸剥夺上调L6细胞A系统活性的机制不同。Western印迹和RT-PCR分析显示，每次刺激后，A系统的蛋白和mRNA水平均升高。
Several studies have demonstrated that the activity of system A is upregulated by insulin, osmotic shock and amino acid deprivation. However, the mechanisms are not clear. We carried out studies using L6 rat skeletal muscle cells to clarify the mechanisms of upregulation of system A activity by insulin, osmotic shock and amino acid deprivation. The upregulation was found to be due to an increase in V (max), not K (m). Chloroquine and wortmannin inhibited the upregulation induced by insulin stimulation and amino acid deprivation but not that induced by osmotic shock. On the other hand, cycloheximide and actinomycin D inhibited the upregulation by each stimulation. Moreover, PD98059 and SP600125 inhibited only amino acid deprivation-induced upregulation and SB202190 inhibited only insulin-induced upregulation. Our findings indicate that the mechanisms of upregulation of system A activity by insulin, osmotic shock and amino acid deprivation are different in L6 cells. Western blot and RT-PCR analysis showed an increase in system A at the protein and mRNA levels with each stimulation.