Trans-Plasma Membrane Electron Transport and Ascorbate Efflux by Skeletal Muscle.
Trans-Plasma Membrane Electron Transport and Ascorbate Efflux by Skeletal Muscle.
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DOI：
10.3390/antiox6040089
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发表时间：
2017-11-09
期刊：
影响因子：
--
通讯作者：
Fisher JS
中科院分区：
文献类型：
--
作者：
Eccardt AM;Bell TP;Mattathil L;Prasad R;Kelly SC;Fisher JS
据报道，跨质膜电子传递（tPMET）和抗坏血酸的抗氧化作用在保护细胞免受活性氧损伤方面发挥着作用，活性氧与引起代谢功能障碍（例如胰岛素抵抗）有关。骨骼肌包含最大的全身器官部分，表明 tPMET 和抗坏血酸输出作为细胞外抗氧化剂的主要来源的潜在作用。我们假设骨骼肌能够进行 tPMET 和抗坏血酸流出。为了测量这些过程，我们检测了培养的肌肉细胞、卫星细胞以及分离的趾长伸肌 (EDL) 和比目鱼肌 (SOL) 还原两种细胞外电子受体、水溶性四唑盐 1 (WST-1) 和二氯酚靛酚 (DPIP) 的能力。利用抗坏血酸氧化酶 (AO) 来确定 WST-1 还原的哪一部分依赖于抗坏血酸流出。我们发现肌肉细胞可以减少细胞外电子受体。在 C2C12 肌管和卫星细胞中，这种减少的很大一部分取决于抗坏血酸。在肌管中，葡萄糖转运蛋白 1 (GLUT1) 抑制剂与泛 GLUT 抑制剂一起抑制 tPMET 和抗坏血酸流出，而 GLUT4 抑制剂则没有效果。腺苷 5'-单磷酸 (AMP) 激活的蛋白激酶激活剂 5-氨基咪唑-4-甲酰胺核糖核苷酸 (AICAR) 可抑制肌管的 tPMET 和抗坏血酸流出，而胰岛素则没有影响。综上所述，我们的数据表明，肌肉细胞能够在 GLUT1 支持下进行 tPMET 和抗坏血酸流出，从而说明了静息肌肉向细胞外环境输出电子和抗氧化剂的模型。
Trans-plasma membrane electron transport (tPMET) and the antioxidant roles of ascorbate reportedly play a role in protection of cells from damage by reactive oxygen species, which have been implicated in causing metabolic dysfunction such as insulin resistance. Skeletal muscle comprises the largest whole-body organ fraction suggesting a potential role of tPMET and ascorbate export as a major source of extracellular antioxidant. We hypothesized that skeletal muscle is capable of tPMET and ascorbate efflux. To measure these processes, we assayed the ability of cultured muscle cells, satellite cells, and isolated extensor digitorum longus (EDL) and soleus (SOL) to reduce two extracellular electron acceptors, water soluble tetrazolium salt 1 (WST-1), and dichlorophenolindophenol (DPIP). Ascorbate oxidase (AO) was utilized to determine which portion of WST-1 reduction was dependent on ascorbate efflux. We found that muscle cells can reduce extracellular electron acceptors. In C2C12 myotubes and satellite cells, a substantial portion of this reduction was dependent on ascorbate. In myotubes, glucose transporter 1 (GLUT1) inhibitors along with a pan-GLUT inhibitor suppressed tPMET and ascorbate efflux, while a GLUT4 inhibitor had no effect. The adenosine 5′-monophosphate (AMP)-activated protein kinase activator 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) suppressed both tPMET and ascorbate efflux by myotubes, while insulin had no effect. Taken together, our data suggest that muscle cells are capable of tPMET and ascorbate efflux supported by GLUT1, thus illustrating a model in which resting muscle exports electrons and antioxidant to the extracellular environment.
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影响因子：
4.1
作者：
GUMAA, KA;MCLEAN, P
通讯作者：
MCLEAN, P
DOI：
10.1016/s1387-2656(05)11004-7
发表时间：
2005-01-01
期刊：
BIOTECHNOLOGY ANNUAL REVIEW, VOL 11
影响因子：
--
作者：
Berridge, MV;Herst, PM;Tan, AS
通讯作者：
Tan, AS
影响因子：
11.4
作者：
Andrisse, Stanley;Koehler, Rikki M.;Chen, Joseph E.;Patel, Gaytri D.;Vallurupalli, Vivek R.;Ratliff, Benjamin A.;Warren, Daniel E.;Fisher, Jonathan S.
通讯作者：
Fisher, Jonathan S.
影响因子：
8.2
作者：
Berti, L;Kellerer, M;Haring, HU
通讯作者：
Haring, HU
影响因子：
4.2
作者：
KAHN, BB
通讯作者：
KAHN, BB