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首页> 外文期刊>American Journal of Physiology >Heterotrimeric G protein Gi is involved in a signal transduction pathway for ATP release from erythrocytes.
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Heterotrimeric G protein Gi is involved in a signal transduction pathway for ATP release from erythrocytes.

机译：异三聚体G蛋白Gi参与红细胞释放ATP的信号转导途径。

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摘要

Erythrocytes are reported to release ATP in response to mechanical deformation and decreased oxygen tension. Previously we proposed that receptor-mediated activation of the heterotrimeric G protein G(s) resulted in ATP release from erythrocytes. Here we investigate the hypothesis that activation of heterotrimeric G proteins of the G(i) subtype are also involved in a signal transduction pathway for ATP release from rabbit erythrocytes. Heterotrimeric G proteins G(alphai1), G(alphai2), and G(alphai3) but not G(alphao) were identified in rabbit and human erythrocyte membranes. Pretreatment of rabbit erythrocytes with pertussis toxin (100 ng/ml, 2 h), which uncouples G(i/o) from their effector proteins, inhibited deformation-induced ATP release. Incubation of rabbit and human erythrocytes with mastoparan (Mas, 10 microM) or Mas-7 (1 microM), which are compounds that directly activate G(i) proteins, resulted in ATP release. However, rabbit erythrocytes did not release ATP when incubated with Mas-17 (10 microM), which is an inactive Mas analog. In separate experiments, Mas (10 microM) but not Mas-17 (10 microM) increased intracellular concentrations of cAMP when incubated with rabbit erythrocytes. Importantly, Mas-induced ATP release from rabbit erythrocytes was inhibited after treatment with pertussis toxin (100 ng/ml, 2 h). These data are consistent with the hypothesis that the heterotrimeric G protein G(i) is a component of a signal transduction pathway for ATP release from erythrocytes.
机译：据报道，红细胞响应机械变形和降低的氧气张力释放ATP。先前我们提出异源三聚体G蛋白G（s）的受体介导的激活导致红细胞释放ATP。在这里，我们调查的假说，G（i）亚型的异源三聚体G蛋白的激活也参与了兔红细胞ATP释放的信号转导途径。异三聚体G蛋白G（alphai1），G（alphai2）和G（alphai3），但在兔和人的红细胞膜中未发现G（alphao）。百日咳毒素（100 ng / ml，2 h）预处理兔红细胞，可将G（i / o）与效应蛋白解偶联，从而抑制了变形诱导的ATP释放。将马索帕兰（Mas，10 microM）或Mas-7（1 microM）（直接激活G（i）蛋白的化合物）与兔和人的红细胞一起孵育，会导致ATP释放。然而，当与Mas-17（10 microM）（一种无活性的Mas类似物）孵育时，兔红细胞不会释放ATP。在单独的实验中，当与兔红细胞孵育时，Mas（10 microM）而不是Mas-17（10 microM）增加了细胞内cAMP浓度。重要的是，用百日咳毒素（100 ng / ml，2 h）处理后，Mas诱导的兔红细胞ATP释放被抑制。这些数据与以下假设相符：异三聚体G蛋白G（i）是红细胞释放ATP的信号转导途径的组成部分。

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