Effect of systemic administration of lipopolysaccharides derived from Porphyromonas gingivalis on gene expression in mice kidney
Effect of systemic administration of lipopolysaccharides derived from Porphyromonas gingivalis on gene expression in mice kidney
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DOI：
10.1007/s00795-018-0181-3
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发表时间：
2018-09-01
影响因子：
1.8
通讯作者：
Abiko, Yoshihiro
中科院分区：
文献类型：
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作者：
Harada, Fumiya;Uehara, Osamu;Abiko, Yoshihiro
虽然牙周炎和慢性肾脏病（CKD）之间的关联已被提出，涉及的机制仍不清楚。在此，我们研究了小鼠模型中的整体基因表达谱，该小鼠模型显示在用来自牙龈卟啉单胞菌（PG-LPS）的脂多糖（LPS）刺激后肾脏中没有急性炎症。给小鼠腹腔注射PG-LPS，浓度为5 mg/kg，每3天一次，持续1个月。微阵列分析用于鉴定在PG-LPS刺激的肾脏中具有最高表达水平的10个基因。其中，已知5个基因（Saa 3、Ticam 2、Reg 3b、Ocxt 2a和Xcr 1）的功能。定量聚合酶链反应分析证实了这些基因的上调。此外，我们研究了这些上调基因的表达是否在体外肾脏来源的内皮细胞中发生改变。实验组中所有五种基因的mRNA表达水平均显著高于对照组（无LPS刺激; *p < 0.05）。总之，肾脏中观察到的反应可能主要来自内皮细胞。此外，Saa 3、Ticam 2、Reg 3b、Ocxt 2a和Xcr 1的表达水平上调可能与CKD的发病机制相关。
Although an association between periodontitis and chronic kidney disease (CKD) has been suggested, the mechanism involved remains unclear. Herein, we examined the global gene expression profile in a mouse model that showed no acute inflammation in the kidney following stimulation with lipopolysaccharides (LPS) derived from Porphyromonas gingivalis (PG-LPS). The mice were injected with PG-LPS at a concentration of 5 mg/kg intraperitoneally, every 3 days, for 1 month. Microarray analysis was used to identify 10 genes with the highest expression levels in the kidney stimulated with PG-LPS. Among them, the functions of five genes (Saa3, Ticam2, Reg3b, Ocxt2a, and Xcr1) were known. The upregulation of these genes was confirmed by quantitative polymerase chain reaction assay. Furthermore, we examined whether the expression of these upregulated genes were altered in endothelial cells derived from the kidney, in vitro. The mRNA expression levels of all five genes were significantly higher in the experimental group than in the controls (no LPS stimulation; *p < 0.05). In conclusion, the responses noted in the kidney may have arisen mainly from the endothelial cells. Moreover, upregulation of the expression levels of Saa3, Ticam2, Reg3b, Ocxt2a, and Xcr1 may be associated with the pathogenesis of CKD.