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Selenium deficiency exacerbates LPS-induced necroptosis by regulating miR-16-5p targeting PI3K in chicken tracheal tissue.
Metallomics ( IF 2.9 ) Pub Date : 2020-03-03 , DOI: 10.1039/c9mt00302a Lanqiao Wang 1 , Xu Shi , Shufang Zheng , Shiwen Xu
Metallomics ( IF 2.9 ) Pub Date : 2020-03-03 , DOI: 10.1039/c9mt00302a Lanqiao Wang 1 , Xu Shi , Shufang Zheng , Shiwen Xu
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Multiple tissue necrosis is one of the morphological features of selenium deficiency-mediated injury. MicroRNA (miRNA) participates in the occurrence and development of necroptosis by regulating target genes. Necroptosis is a programmed form of necrosis, and it is closely related to lipopolysaccharide (LPS)-induced injury. Our aim was to investigate whether Se deficiency can promote tracheal injury caused by LPS through miRNA-induced necroptosis. By establishing models of tracheal injury in Se-deficient chickens, we verified the targeting relationship between chicken-derived miR-16-5p and PI3K through bioinformatics, qRT-PCR and WB analyses, and we measured the changes in the expression of genes related to the PI3K/AKT pathway, RIP3/MLKL pathway and MAPK pathway and of heat shock proteins. Under the condition of Se deficiency, the following results were observed: PI3K/AKT expression decreased with the upregulation of miR-16-5p, the expression of necroptosis-related factors (TNF-α, RIP1, FADD, RIP3 and MLKL) increased, and the expression of Caspase 8 significantly decreased (p < 0.05). Light microscopy observations indicated that cell necrosis was the main pathological change due to Se deficiency injury in the tracheal epithelium. The MAPK pathway was activated, and HSP expression was upregulated, indicating that the MAPK pathway and HSPs are both involved in Se deficiency-mediated necroptosis. In addition, Se deficiency promoted the expression of necroptosis-related genes in LPS-treated chickens (p < 0.05), and the pathological changes of cell necrosis were more obvious. In conclusion, we demonstrated that Se deficiency regulates the miR-16-5p-PI3K/AKT pathway and exacerbates LPS-induced necroptosis in chicken tracheal epithelial cells by activating necroptosis-related genes.
中文翻译：
硒缺乏症通过调节针对气管组织中PI3K的miR-16-5p来加剧LPS诱导的坏死性肾病。
多组织坏死是硒缺乏介导的损伤的形态学特征之一。MicroRNA（miRNA）通过调节靶基因参与坏死病的发生和发展。坏死性坏死是一种程序性的坏死形式，它与脂多糖（LPS）引起的损伤密切相关。我们的目的是研究硒缺乏症是否可以通过miRNA诱导的坏死性硬化促进LPS引起的气管损伤。通过建立硒缺乏鸡的气管损伤模型，我们通过生物信息学，qRT-PCR和WB分析验证了鸡源miR-16-5p和PI3K的靶向关系，并测量了与之相关的基因表达的变化PI3K / AKT途径，RIP3 / MLKL途径和MAPK途径以及热激蛋白。在硒缺乏的情况下 观察到以下结果：PI3K / AKT表达随着miR-16-5p的上调而降低，坏死病相关因子（TNF-α，RIP1，FADD，RIP3和MLKL）的表达增加，而Caspase 8的表达显着增加降低（p <0.05）。光学显微镜观察表明，气管上皮中硒缺乏症引起的细胞坏死是主要的病理改变。MAPK途径被激活，HSP表达上调，表明MAPK途径和HSPs均与硒缺乏介导的坏死病有关。此外，硒缺乏促进了LPS处理的鸡中坏死病相关基因的表达（p <0.05），细胞坏死的病理变化更为明显。结论，
更新日期：2020-02-26
中文翻译：
硒缺乏症通过调节针对气管组织中PI3K的miR-16-5p来加剧LPS诱导的坏死性肾病。
多组织坏死是硒缺乏介导的损伤的形态学特征之一。MicroRNA（miRNA）通过调节靶基因参与坏死病的发生和发展。坏死性坏死是一种程序性的坏死形式，它与脂多糖（LPS）引起的损伤密切相关。我们的目的是研究硒缺乏症是否可以通过miRNA诱导的坏死性硬化促进LPS引起的气管损伤。通过建立硒缺乏鸡的气管损伤模型，我们通过生物信息学，qRT-PCR和WB分析验证了鸡源miR-16-5p和PI3K的靶向关系，并测量了与之相关的基因表达的变化PI3K / AKT途径，RIP3 / MLKL途径和MAPK途径以及热激蛋白。在硒缺乏的情况下 观察到以下结果：PI3K / AKT表达随着miR-16-5p的上调而降低，坏死病相关因子（TNF-α，RIP1，FADD，RIP3和MLKL）的表达增加，而Caspase 8的表达显着增加降低（p <0.05）。光学显微镜观察表明，气管上皮中硒缺乏症引起的细胞坏死是主要的病理改变。MAPK途径被激活，HSP表达上调，表明MAPK途径和HSPs均与硒缺乏介导的坏死病有关。此外，硒缺乏促进了LPS处理的鸡中坏死病相关基因的表达（p <0.05），细胞坏死的病理变化更为明显。结论，
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