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Switching off HSP70 and i-NOS to study their role in normal and H2O2-stressed human fibroblasts

机译：关闭HSP70和i-NOS，以研究它们在正常和H2O2胁迫下的人成纤维细胞中的作用

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i-NOS and HSP70 antisense oligonucleotides were used to study the role of the two well known stress-regulated molecules on cell survival of both untreated control, and H2O2-stressed human fibroblasts. Cell survival was assessed either by LDH release or by MTT assay. The levels of cytosolic i-NOS and HSP70 were tested by using immunoblotting analysis, and reactive oxygen species (ROS) production was quantified. Compared to the values observed in untreated control cells, anti HSP70-transfected human fibroblasts showed an increase in ROS production, i-NOS level and LDH release. The addition of 0.12 mM H2O2 for 20 min. to the HSP70-deprived fibroblasts did not modify the percentage of LDH release observed in H2O2 stressed cells, but reduced cell viability increasing both ROS production and i-NOS level. Anti i-NOS-transfected fibroblasts, compared to the control untreated cells, showed no modification in ROS production, while cell survival was improved. When treated with H2O2 the i-NOS depleted cells counteracted ROS formation as well as LDH release but negatively affected cell viability and HSP70 levels, compared to the results obtained with H2O2 alone-treated fibroblasts. The data indicates that the induced decrease in HSP70 level in oxidative stress conditions makes fibroblasts more prone to oxidative injury and also increases i-NOS level. Whereas in one way the forced decrease in i-NOS expression seems to counteract ROS production stimulated by the oxidative insult in the cells, in another way, since it causes a decrease in HSP70 expression as well as in cell viability, it seems to activate some unidentified pathways affecting cell demise. (C) 2003 Elsevier Inc. All rights reserved. [References: 52]
机译：使用i-NOS和HSP70反义寡核苷酸研究了两种众所周知的应激调节分子对未经处理的对照和H2O2胁迫的人成纤维细胞的细胞存活的作用。通过LDH释放或MTT测定评估细胞存活。使用免疫印迹分析测试了细胞质i-NOS和HSP70的水平，并对活性氧（ROS）的产生进行了定量。与未处理的对照细胞中观察到的值相比，抗HSP70转染的人成纤维细胞显示ROS产量，i-NOS水平和LDH释放增加。添加0.12 mM H2O2 20分钟。 HSP70剥夺的成纤维细胞对H2O2胁迫的细胞中LDH释放的百分比没有改变，但是降低了细胞活力，增加了ROS的产生和i-NOS的水平。与未处理的对照细胞相比，抗i-NOS转染的成纤维细胞在ROS的产生上没有任何改变，而细胞存活率却得到了改善。与单独使用H2O2处理的成纤维细胞获得的结果相比，当用H2O2处理时，消耗i-NOS的细胞可抵消ROS的形成以及LDH的释放，但对细胞活力和HSP70水平产生负面影响。数据表明，在氧化应激条件下诱导的HSP70水平降低使成纤维细胞更易于发生氧化损伤，同时也增加了i-NOS水平。一方面，i-NOS表达的强迫减少似乎可以抵消细胞中氧化性刺激刺激的ROS产生;另一方面，由于它导致HSP70表达以及细胞活力的减少，因此似乎可以激活一些影响细胞死亡的未知途径。 （C）2003 Elsevier Inc.保留所有权利。 [参考：52]

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