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Increase in Dual specificity phosphatase 1, TGF-beta stimulated gene 22, domain family protein 3 and Luc7 homolog (S. cerevisiae)-like messenger RNA after mechanical asphyxiation in the mouse lung.

机译:机械肺窒息后,双重特异性磷酸酶1,TGF-β刺激的基因22,域家族蛋白3和Luc7同源物(酿酒酵母)样信使RNA的增加。

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We investigated the transcriptome profile of mechanical asphyxia and decapitation at 60min after death using serial analysis of gene expression. After comparing the results, 11 genes were significantly increased by the mechanical asphyxia treatment in the mouse lung. Of those genes, quantitative real-time PCR revealed that Dual specificity phosphatase 1 (Dusp1), TGF-beta stimulated gene 22, domain family protein 3 (TSC22d3) and Luc7 homolog (Saccharomyces cerevisiae)-like (Luc7l) after asphyxia were more significantly increased than those after decapitation. Dusp1 inactivated mitogen activated protein kinase, which functions in cell proliferation. However, the consumption of oxygen had a disadvantageous effect on survival, because tissue or cells were not able to produce energy by internal respiration under the suddenly hypoxic condition following asphyxia. The increased transcripts of Dusp1 following asphyxia suppressed oxygen consumption. TSC22d3 was isolated as a TGF-beta-inducible gene and it is also identified as a glucocorticoid (GC)-induced leucine zipper (GILZ). GC was released from the adrenal gland via HPA axis under the hypoxic condition. Especially in acute suffocation, GC rapidly increased. Therefore, the increase in TSC22d3 may be induced by the increased GC following asphyxia. We were unable to clarify the Luc7l increase, because there are no reports in relation to asphyxia. In addition, GILZ mediates the antiproliferative activity of glucocorticoids. We thought that the increasing TSC22d3 may lead to the suppression of oxygen consumption to avoid wasting energy, as in proliferation, the same as the increase in Dusp1. Our data indicated that the determination of the protein product level in the lung could help in diagnosing asphyxia. In addition, these data may contribute to revealing the patho-physiology of asphyxia and to help diagnose asphyxia, including hanging.
机译:我们使用基因表达的系列分析调查了死亡后60分钟时机械性窒息和断头的转录组概况。比较结果后,通过机械性窒息治疗小鼠肺中11个基因显着增加。在这些基因中,实时荧光定量PCR显示,窒息后双重特异性磷酸酶1(Dusp1),TGF-β刺激的基因22,结构域家族蛋白3(TSC22d3)和Luc7同源物(酿酒酵母)样(Luc7l)更为显着。比斩首之后增加了Dusp1使丝裂原活化的蛋白激酶失活,该蛋白激酶在细胞增殖中起作用。然而,氧气的消耗对生存有不利影响,因为在窒息后突然缺氧的情况下,组织或细胞无法通过内部呼吸产生能量。窒息后Dusp1的转录增加抑制了氧气的消耗。 TSC22d3作为TGF-β诱导型基因被分离,并且还被鉴定为糖皮质激素(GC)诱导的亮氨酸拉链(GILZ)。在缺氧条件下,通过HPA轴从肾上腺释放GC。特别是在急性窒息中,GC迅速增加。因此,窒息后GC升高可能导致TSC22d3升高。由于没有关于窒息的报道,我们无法阐明Luc7l的增加。此外,GILZ介导了糖皮质激素的抗增殖活性。我们认为增加TSC22d3可能会导致抑制耗氧量,从而避免浪费能量(与扩散一样),与Dusp1的增加相同。我们的数据表明,确定肺中蛋白质产物水平可以帮助诊断窒息。此外,这些数据可能有助于揭示窒息的病理生理,并有助于诊断窒息,包括悬挂。

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