Nitric oxide induces metallothionein-I gene expression in mesangial cells.
Nitric oxide induces metallothionein-I gene expression in mesangial cells.
复制标题
DOI：
10.1016/j.trsl.2006.04.002
复制
发表时间：
2006-10-01
期刊：
影响因子：
--
通讯作者：
Lianos, Elias A
中科院分区：
文献类型：
--
作者：
Datta, Prasun K;Lianos, Elias A
在涉及肾小球的各种形式的损伤中，系膜细胞暴露于由一氧化氮合酶（NOS）的诱导型同种型的活化引起的潜在毒性浓度的一氧化氮（NO）。系膜细胞是否具有防御NO介导的氧化损伤的系统尚不清楚。一个公认的系统是金属硫蛋白（MT）。金属硫蛋白是半胱氨酸蛋白家族中的一员，具有重要的抗氧化作用。作者评估了NO是否上调培养的肾小球系膜细胞中MT-I的表达。北方印迹分析显示，三种不同的NO供体：硝普钠（SNP）、S-亚硝基-N-乙酰基-DL-青霉胺（SNAP）和精胺-NONOate（Sper/NO）可增加稳态MT-I mRNA水平。由SNAP衍生的NO诱导的MT-I mRNA水平的增加被抗氧化剂N-乙酰半胱氨酸（NAC）（谷胱甘肽（GSH）前体）减弱，这表明NO介导的MT-I表达的机制可能涉及氧化应激反应。这些观察确定MT-I作为一个假定的抗氧化系统在NO介导的系膜细胞损伤。
In various forms of injury involving the renal glomerulus, mesangial cells are exposed to potentially toxic concentrations of nitric oxide (NO) caused by activation of the inducible isoform of nitric oxide synthase (NOS). Whether mesangial cells possess systems that can defend against NO mediated oxidative injury is unknown. One putative system is Metallothionein (MT). Metallothioneins constitute a family of cysteine proteins and play a significant role as anti-oxidants. The authors assessed whether NO upregulates MT-I expression in cultured glomerular mesangial cells. Northern blot analysis revealed that steady state MT-I mRNA levels were increased by three different NO donors: sodium nitroprusside (SNP), S-nitroso-N-acetyl-DL-penicillamine (SNAP), and Spermine-NONOate (Sper/NO). The increase in MT-I mRNA levels induced by SNAP-derived NO was attenuated by the antioxidant N-acetylcysteine (NAC), a glutathione (GSH) precursor, which indicates that the mechanism of NO-mediated MT-I expression may involve an oxidative stress response. These observations identify MT-I as a putative antioxidant system in NO-mediated mesangial cell injury.