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首页> 外文期刊>Endothelium: Journal of endothelial cell research >Glutathione-S-transferase protects against oxidative injury of endothelial cell tight junctions.
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Glutathione-S-transferase protects against oxidative injury of endothelial cell tight junctions.

机译：谷胱甘肽-S-转移酶可防止内皮细胞紧密连接的氧化损伤。

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摘要

Oxidative damage of endothelial tight junction permeability is involved in the pathophysiology of a variety of vascular diseases. The authors studied the role of the antioxidant enzyme, human glutathione-S-transferase A4-4 (hGSTA4-4), in regulating expression of major molecules of tight junction in vascular endothelial cells under oxidative stress induced by H(2)O(2). A vascular endothelial cell line, mouse pancreatic endothelial cells (MS1), was transduced with recombinant adenoviral vector containing hGSTA4-4 gene. hGSTA4-4 induced expression of tight junction proteins occludin and zonula occludens (ZO)-1 under oxidative stress. Increased hGSTA4-4 expression correlated with increased transepithelial electrical resistance and decreased tyrosine phosphorylation of occludin and ZO-1 following exposure to H(2)O(2). In addition, morphologic dissociation of occludin, ZO-1, and F-actin during oxidative stress was reduced in hGSTA4-4-expressing cells. To explore a genetic approach for vascular diseases associated with disruption of tight junction proteins, we introduced the same viral vector to blood vessels of mice, rats, and rabbits ex vivo and found strong expression of hGSTA4-4 in endothelial cells. These results demonstrate that oxidative stress mediated disruption of tight junctions in endothelial cells may be attenuated by hGSTA4-4 expression.
机译：内皮紧密连接通透性的氧化损伤涉及多种血管疾病的病理生理。作者研究了抗氧化酶人谷胱甘肽S转移酶A4-4（hGSTA4-4）在调节H（2）O（2）引起的氧化应激下血管内皮细胞紧密连接主要分子表达中的作用）。用含有hGSTA4-4基因的重组腺病毒载体转导血管内皮细胞系，小鼠胰腺内皮细胞（MS1）。 hGSTA4-4诱导氧化应激下紧密连接蛋白occludin和zonula occludens（ZO）-1的表达。增加的hGSTA4-4表达与增加的跨上皮电阻和减少的Occludin和ZO-1的酪氨酸磷酸化后暴露于H（2）O（2）。另外，在表达hGSTA4-4的细胞中，在氧化应激期间，闭合蛋白，ZO-1和F-肌动蛋白的形态学解离减少。为了探索与紧密连接蛋白破坏有关的血管疾病的遗传学方法，我们将相同的病毒载体引入了离体小鼠，大鼠和兔子的血管中，并发现hGSTA4-4在内皮细胞中的强表达。这些结果证明，hGSTA4-4表达可以减轻氧化应激介导的内皮细胞紧密连接的破坏。

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