Regulation of manganese superoxide dismutase: IL-1 and TNF induction in pulmonary artery and microvascular endothelial cells.
Regulation of manganese superoxide dismutase: IL-1 and TNF induction in pulmonary artery and microvascular endothelial cells.
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DOI：
10.1016/0006-291x(92)92406-n
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发表时间：
1992-10
影响因子：
3.1
通讯作者：
G. Visner;S. Chesrown;J. Monnier;U. Ryan;H. Nick
中科院分区：
文献类型：
--
作者：
G. Visner;S. Chesrown;J. Monnier;U. Ryan;H. Nick
IL-1和TNF是炎症反应中的重要介质，并与肺内皮细胞损伤有关。肿瘤坏死因子和白介素1细胞介导的损伤被认为是通过增加细胞内氧自由基的产生而发生的。然而，这些细胞因子也被证明可以保护肺免受高氧介导的氧化剂损伤。本文研究了大鼠肺动脉和微血管内皮细胞中抗氧化酶MnSOD和铜/锌超氧化物歧化酶对IL-1、肿瘤坏死因子和内毒素的反应。这些介体可增加两种大鼠肺内皮细胞MnSOD的表达，但不增加铜/锌超氧化物歧化酶的表达。细胞因子与脂多糖共同作用时，可观察到一种相加效应。MnSOD mRNA的诱导依赖于转录事件，但不需要从头合成蛋白质。
IL-1 and TNF are important mediators in the inflammatory response, and have been associated with endothelial cell damage in the lung. TNF and IL-1 cell-mediated injury has been proposed to occur through an increase in intracellular oxygen free radical production. However, these cytokines have also been shown to protect the lung from hyperoxia-mediated oxidant injury. In this paper we evaluated the response of the antioxidant enzymes, MnSOD and Cu/ZnSOD to IL-1, TNF, and LPS in both rat pulmonary artery and microvascular endothelial cells. These mediators produced an increase in MnSOD but not Cu/ZnSOD expression in both rat pulmonary endothelial cells. An additive effect was observed with co-treatment by the cytokines with LPS. The MnSOD mRNA induction is dependent upon a transcriptional event, but did not require de novo protein synthesis.