Gao Qinling, Yuan Shuhua, Yuan Dawei
Second Department of Pediatric Internal Medicine, Linyi People's Hospital, Linyi, China.
Department of Neonatology, Linyi People's Hospital, Linyi, China.
Minerva Pediatr. 2018 Oct;70(5):438-443. doi: 10.23736/S0026-4946.17.04921-0. Epub 2017 Sep 15.
We explored the correlation between the TGFBR2 gene that is mediated by NF-κb signaling pathways and the pathogenesis of Kawasaki disease in children.
In this study, 43 children with Kawasaki disease from April 2014 to January 2016 at our hospital were selected as the observation group, and 42 healthy children were selected as the control group. The mRNA expression levels of NF-κb gene and TGFBR2 gene in different groups were detected using fluorescence quantitative PCR. The protein expression levels of the NF-κb and TGFBR2 were detected using enzyme-linked immunosorbent assay (ELISA) in different groups. The expression levels of NF-κb and TGFBR2 in the observation group and the control group were detected using immunohistochemistry.
Compared to the control group, the mRNA expression levels of NF-κb and TGFBR2 were 12.3 times and 27.5 times as high as those in the control group respectively and there were significant differences between the two groups (P<0.05). ELISA results showed that there were significant differences between the protein expression levels of NF-κb and TGFBR2 in the control group (0.87±0.12, 1.25±0.18 µg/L) and those in the observation group (3.27±0.17, 8.16±0.22 µg/L) (P<0.05). Western-blotting results showed that the expression levels of the NF-κB and TGFBR2 in children with Kawasaki disease were significantly higher than those in healthy subjects (P<0.05). Immunohistochemistry results showed that the positive cell rate of TGFBR2 (89.7%) was significantly higher in children with Kawasaki disease than that in healthy children (4.5%); there was significant difference between the two groups (P<0.05).
The TGFBR2 may be involved in the pathogenesis of Kawasaki disease in children through NF-κb signaling pathways.
我们探讨了由核因子κB(NF-κb)信号通路介导的转化生长因子β受体2(TGFBR2)基因与儿童川崎病发病机制之间的相关性。
本研究选取2014年4月至2016年1月在我院就诊的43例川崎病患儿作为观察组,选取42例健康儿童作为对照组。采用荧光定量聚合酶链反应(PCR)检测不同组中NF-κb基因和TGFBR2基因的mRNA表达水平。采用酶联免疫吸附测定(ELISA)检测不同组中NF-κb和TGFBR2的蛋白表达水平。采用免疫组织化学法检测观察组和对照组中NF-κb和TGFBR2的表达水平。
与对照组相比,NF-κb和TGFBR2的mRNA表达水平分别是对照组的12.3倍和27.5倍,两组间差异有统计学意义(P<0.05)。ELISA结果显示,对照组(0.87±0.12,1.25±0.18μg/L)和观察组(3.27±0.17,8.16±0.22μg/L)中NF-κb和TGFBR2的蛋白表达水平差异有统计学意义(P<0.05)。蛋白质印迹法结果显示,川崎病患儿中NF-κB和TGFBR2的表达水平显著高于健康受试者(P<0.05)。免疫组织化学结果显示,川崎病患儿中TGFBR2的阳性细胞率(89.7%)显著高于健康儿童(4.5%);两组间差异有统计学意义(P<0.05)。
TGFBR2可能通过NF-κb信号通路参与儿童川崎病的发病机制。