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首页> 外文期刊>Molecular biology of the cell >Insulin and hypertonicity recruit GLUT4 to the plasma membrane of muscle cells by using N-ethylmaleimide-sensitive factor-dependent SNARE mechanisms but different v-SNAREs: Role of TI-VAMP
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Insulin and hypertonicity recruit GLUT4 to the plasma membrane of muscle cells by using N-ethylmaleimide-sensitive factor-dependent SNARE mechanisms but different v-SNAREs: Role of TI-VAMP

机译：胰岛素和高渗性通过使用N-乙基马来酰亚胺敏感因子依赖性SNARE机制，但使用不同的v-SNARE，将GLUT4募集到肌肉细胞的质膜上：TI-VAMP的作用

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Insulin and hypertonicity each increase the content of GLUT4 glucose transporters at the surface of muscle cells. Insulin enhances GLUT4 exocytosis without diminishing its endocytosis. The insulin but not the hypertonicity response is reduced by tetanus neurotoxin, which cleaves vesicle-associated membrane protein (VAMP)2 and VAMP3, and is rescued upon introducing tetanus neurotoxin-resistant VAMP2. Here, we show that hypertonicity enhances GLUT4 recycling, compounding its previously shown ability to reduce GLUT4 endocytosis. To examine whether the canonical soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) mechanism is required for the plasma membrane fusion of the tetanus neurotoxin-insensitive GLUT4 vesicles, L6 myoblasts stably expressing myc-tagged GLUT4 (GLUT4myc) were transiently transfected with dominant negative N-ethylmaleimide-sensitive factor (NSF) (DN-NSF) or small-interfering RNA to tetanus neurotoxin-insensitive VAMP (TI-VAMP siRNA). Both strategies markedly reduced the basal level of surface GLUT4myc and the surface gain of GLUT4myc in response to hypertonicity. The insulin effect was abolished by DN-NSF, but only partly reduced by TI-VAMP siRNA. We propose that insulin and hypertonicity recruit GLUT4myc from partly overlapping, but distinct sources defined by VAMP2 and TI-VAMP, respectively.
机译：胰岛素和高渗性都会增加肌肉细胞表面GLUT4葡萄糖转运蛋白的含量。胰岛素可增强GLUT4的胞吐作用，而不会减少其内吞作用。破伤风神经毒素可减少胰岛素，但不会引起高渗反应，该酶可裂解囊泡相关膜蛋白（VAMP）2和VAMP3，并在引入抗破伤风神经毒素的VAMP2后得以拯救。在这里，我们表明高渗增强了GLUT4的循环利用，增强了其先前显示的减少GLUT4内吞作用的能力。为了检查破伤风对神经毒素不敏感的GLUT4囊泡的质膜融合是否需要标准的可溶性N-乙基马来酰亚胺敏感因子附着蛋白受体（SNARE）机制，将稳定表达myc标记的GLUT4（GLUT4myc）的L6成肌细胞瞬时转染了对破伤风神经毒素不敏感的VAMP（TI-VAMP siRNA）具有显性负性N-乙基马来酰亚胺敏感因子（NSF）（DN-NSF）或小干扰RNA。两种策略均显着降低了表面高渗的基础GLUT4myc的基础水平和GLUT4myc的表面增益。 DN-NSF消除了胰岛素作用，但TI-VAMP siRNA仅部分减弱了胰岛素作用。我们建议胰岛素和高渗性从部分重叠但分别由VAMP2和TI-VAMP定义的不同来源募集GLUT4myc。

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