Nitric oxide-induced reduction of lung cell and whole lung thioredoxin expression is regulated by NF-kappaB.
Nitric oxide-induced reduction of lung cell and whole lung thioredoxin expression is regulated by NF-kappaB.
复制标题
一氧化氮诱导的肺细胞和全肺硫氧还蛋白表达减少受 NF-κB 调节。
DOI：
10.1152/ajplung.1999.277.4.l787
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Block,ER
中科院分区：
文献类型：
--
作者：
Zhang,J;Velsor,LW;Patel,JM;Postlethwait,EM;Block,ER
We examined whether nitric oxide (NO)-induced inhibition of thioredoxin (Thx) expression is regulated by a mechanism mediated by a transcription factor, i.e., nuclear factor-κB (NF-κB), in cultured porcine pulmonary artery endothelial cells (PAEC) and in mouse lungs. Western blot analysis revealed that IκB-α content was reduced by 20 and 60% in PAEC exposed to 8.5 ppm NO for 2 and 24 h, respectively. NO exposure also caused significant reductions of cytosol fraction p65 and p52 content in PAEC. The nuclear fraction p65 and p52 contents were significantly reduced only in PAEC exposed to NO for 24 h. Exposure to NO resulted in a 50% reduction of p52 mRNA but not of the IκB-α subunit. DNA binding activity of the oligonucleotide encoding the NF-κB sequence in theThxgene was significantly reduced in PAEC exposed to NO for 24 h. Exposure of mice to 10 ppm NO for 24 h resulted in a significant reduction of lung Thx and IκB-α mRNA and protein expression and in the oligonucleotide encoding Thx and NF-κB/DNA binding. These results1) demonstrate that the effects of NO exposure on Thx expression in PAEC are comparable to those observed in intact lung and2) suggest that reduced expression of the NF-κB subunit, leading to reduced NF-κB/DNA binding, is associated with the loss of Thx expression in PAEC and in intact mouse lungs.
