LINC00667调控NF-κB信号通路对高糖诱导的人近端肾小管上皮细胞EMT的影响  

Effect of LINC00667 on EMT of High Glucose Induced Human Proximal Renal Tubular Epithelial Cells by Regulating NF-κB Signaling Pathway

作　　者：张彦 金进 王黎 王玉梅[2] ZHANG Yan;JIN Jin;WANG Li(Department of Endocrinology,People’s Hospital of Dongxihu District,Wuhan 430040)

机构地区：[1]湖北省武汉市东西湖区人民医院内分泌科,武汉430040 [2]华中科技大学同济医学院附属协和医院肾内科,武汉430022

出　　处：《中国中西医结合肾病杂志》2021年第7期575-578,共4页Chinese Journal of Integrated Traditional and Western Nephrology

基　　金：湖北省自然科学基金项目(No.WJ2015MB013)。

摘　　要：目的:探讨LINC00667对高糖诱导的人近端肾小管上皮细胞间充质转化(EMT)及核因子κB(NF-κB)信号通路的影响。方法:将人肾小管上皮细胞HK-2分为正常对照(NC)组、高糖(HG)组、HG+si-con组、HG+si-LINC00667组、HG+si-LINC00667+PBS组、HG+si-LINC00667+TNF-α组。实时荧光定量PCR(RT-qPCR)检测LINC00667的表达;酶联免疫吸附测定(ELISA)试剂盒检测白细胞介素1β(IL-1β)和转化生长因子(TGF-β_(1))含量;蛋白质印记(Western blot)检测钙黏蛋白(E-cadherin)、波形蛋白(Vimentin)、α-平滑肌肌动蛋白(α-SMA)以及NF-κB信号通路相关蛋白的表达。结果:与NC组比较,HG组HK-2细胞LINC00667、Vimentin和α-SMA表达升高,E-cadherin表达降低,细胞培养液上清中IL-1β和TGF-β_(1)含量升高,NF-κB信号通路激活(P<0.05)。与HG+si-con组比较,HG+si-LINC00667组HK-2细胞Vimentin和α-SMA表达降低,E-cadherin表达升高,细胞培养液上清中IL-1β和TGF-β_(1)含量降低,NF-κB信号通路受到抑制(P<0.05)。与HG+si-LINC00667+PBS组比较,HG+si-LINC00667+TNF-α组HK-2细胞NF-κB信号通路激活,Vimentin和α-SMA表达升高,E-cadherin表达降低,细胞培养液上清中IL-1β和TGF-β_(1)含量升高(P<0.05)。结论:沉默LINC00667可抑制高糖诱导的人近端肾小管上皮细胞EMT,抑制炎症反应,其机制与抑制NF-κB信号通路有关。Objective:To investigate the effect of LINC00667 on high glucose-induced mesenchymal transition(EMT)and nuclear factor-κB(NF-κB)signaling pathway in human proximal renal tubular epithelial cells.Methods:Human renal tubular epithelial cells HK-2 were divided into normal control(NC)group,high glucose(HG)group,HG+si-con group,HG+si-LINC00667 group,HG+si-LINC00667+PBS group,HG+si-LINC00667+TNF-αgroup.Real-time fluorescence quantitative PCR(RT-qPCR)was used to detect the expression of LINC00667;enzyme-linked immunosorbent assay(ELISA)kit was selected to detect the content of interleukin-1β(IL-1β)and transforming growth factor(TGF-β_(1));Western blot was utilized to detect the expression of E-cadherin,vimentin,α-smooth muscle actin(α-SMA)and NF-κB signaling pathway related proteins.Results:Compared with NC group,the expressions of LINC00667,Vimentin andα-SMA increased,the expression of E-cadherin decreased,the contents of IL-1βand TGF-β_(1)in the supernatant increased,and NF-κB Signaling pathway was activated in HG group(P<0.05).Compared with HG+si-con group,the expression of Vimentin andα-SMA decreased,the expression of E-cadherin increased,and the contents of IL-1βand TGF-β_(1)in the cell culture supernatant decreased,the NF-κB signaling pathway was inhibited in HG+si-LINC00667 group(P<0.05).Compared with HG+si-LINC00667+PBS group,the NF-κB signaling pathway was activated,the expression of Vimentin andα-SMA increased,the expression of E-cadherin decreased,and the contents of IL-1βand TGF-β_(1)in the supernatant increased in HG+si-LINC00667+TNF-αgroup(P<0.05).Conclusion:Silencing LINC00667 inhibits high glucose-induced EMT of human proximal renal tubular epithelial cells and inhibit inflammatory responses.The mechanism is related to the inhibition of NF-κB signaling pathway.

关 键 词：LINC00667 高糖 肾小管上皮细胞间充质转化 NF-ΚB信号通路 

分 类 号：R587.2[医药卫生—内分泌] R692.9[医药卫生—内科学]