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首页> 外文期刊>Cytokine >Erythropoietin and hypoxia increase erythropoietin receptor and nitric oxide levels in lung microvascular endothelial cells.
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Erythropoietin and hypoxia increase erythropoietin receptor and nitric oxide levels in lung microvascular endothelial cells.

机译:促红细胞生成素和缺氧会增加肺微血管内皮细胞中的促红细胞生成素受体和一氧化氮水平。

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摘要

Acute lung exposure to low oxygen results in pulmonary vasoconstriction and redistribution of blood flow. We used human microvascular endothelial cells from lung (HMVEC-L) to study the acute response to oxygen stress. We observed that hypoxia and erythropoietin (EPO) increased erythropoietin receptor (EPOR) gene expression and protein level in HMVEC-L. In addition, EPO dose- and time-dependently stimulated nitric oxide (NO) production. This NO stimulation was evident despite hypoxia induced reduction of endothelial NO synthase (eNOS) gene expression. Western blot of phospho-eNOS (serine1177) and eNOS and was significantly induced by hypoxia but not after EPO treatment. However, iNOS increased at hypoxia and with EPO stimulation compared to normal oxygen tension. In accordance with our previous results of NO induction by EPO at low oxygen tension in human umbilical vein endothelial cells and bone marrow endothelial cells, these results provide further evidence in HMVEC-L for EPO regulation of NO production to modify the effects of hypoxia and cause compensatory vasoconstriction.
机译:急性肺暴露于低氧会导致肺血管收缩和血流重新分布。我们使用了来自肺的人类微血管内皮细胞(HMVEC-L)来研究对氧应激的急性反应。我们观察到缺氧和促红细胞生成素(EPO)增加HMVEC-L中的促红细胞生成素受体(EPOR)基因表达和蛋白质水平。此外,EPO剂量和时间依赖性刺激了一氧化氮(NO)的产生。尽管缺氧诱导内皮一氧化氮合酶(eNOS)基因表达降低,但这种NO刺激仍然很明显。磷酸化eNOS(serine1177)和eNOS的Western印迹被缺氧显着诱导,但在EPO处理后没有。但是,与正常的氧气张力相比,在缺氧和EPO刺激下iNOS升高。根据我们先前在低氧张力下人脐静脉内皮细胞和骨髓内皮细胞中EPO诱导NO的结果,这些结果为HMVEC-L提供了进一步的证据,证明EPO可以调节EPO来调节NO的产生,从而改变缺氧的影响并引起代偿性血管收缩。

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