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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >S-nitrosylation and permeation through connexin 43 hemichannels in astrocytes: Induction by oxidant stress and reversal by reducing agents
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S-nitrosylation and permeation through connexin 43 hemichannels in astrocytes: Induction by oxidant stress and reversal by reducing agents

机译：S-亚硝基化和星形胶质细胞中通过连接蛋白43半通道的渗透：氧化应激诱导和还原剂逆转

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摘要

Marked increase in cell permeability ascribed to open connexin (Cx)43 hemichannels is induced by metabolic inhibition (MI) of cortical astrocytes in culture, but the molecular mechanisms are not established. Dephosphorylation and/or oxidation of Cx43 hemichannels was proposed as a potential mechanism to increase their open probability. We now demonstrate that Ml increases the number of hemichannels on the cell surface assayed by biotinyla-tion and Western blot, and that this change is followed by increased dephosphorylation and S-nitrosylation. The increase in rate of dye uptake caused by Ml is comparable to the increase in surface expression; thus, open probability and permeation per hemichannel may be unchanged. Reducing agents did not affect dephosphorylation of Cx43 hemichannels but reduced dye uptake and S-nitrosylation. Uptake was also reduced by elevated intra-cellular but not extracellular levels of reduced glutathione. Moreover, nitric oxide donors induced dye uptake and nitrosylation of surface Cx43 but did not affect its abundance or phosphorylation. Thus, permeability per channel is increased, presumably because of increase in open probability. We propose that increased dye uptake induced by Ml is mediated by an increased number of Cx43 hemichannels in the surface and is associated with multiple molecular changes, among which nitrosylation of intracellular Cx43 cysteine residues may be a critical factor.
机译：培养的皮质星形胶质细胞的代谢抑制（MI）可诱导归因于开放连接蛋白（Cx）43半通道的细胞通透性显着增加，但尚未建立分子机制。 Cx43半通道的去磷酸化和/或氧化被认为是增加其开放可能性的潜在机制。现在我们证明，M1增加了通过生物素化和Western印迹分析的细胞表面上半通道的数量，并且该变化之后是增加的去磷酸化和S-亚硝基化。由M1引起的染料摄取速率的增加可与表面表达的增加相媲美。因此，每个半通道的开放概率和渗透率可能不变。还原剂不会影响Cx43半通道的去磷酸化，但会减少染料吸收和S-亚硝基化。谷胱甘肽减少的细胞内水平但不是细胞外水平的升高也减少了摄取。此外，一氧化氮供体诱导了表面Cx43的染料吸收和亚硝基化，但不影响其丰度或磷酸化。因此，每个通道的渗透性增加了，大概是由于开放概率的增加。我们提出由M1诱导的染料摄取的增加是由表面中Cx43半通道数目的增加所介导的，并且与多种分子变化有关，其中细胞内Cx43半胱氨酸残基的亚硝基化可能是关键因素。

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