| 万笑笑.miR-216a抑制 Kruppel样转录因子9调控核因子-κB信号通路对肾小管上皮细胞急性肾损伤的影响[J].安徽医药,2020,24(9):1791-1795. |
| miR-216a抑制 Kruppel样转录因子9调控核因子-κB信号通路对肾小管上皮细胞急性肾损伤的影响 |
| Effect of mi-216a on acute renal injury in renal tubular epithelial cells via inhibition of Kruppel-like transcription factor 9 and regulation of nuclear factor-kB signaling pathway |
| |
| DOI：10.3969/j.issn.1009-6469.2020.09.024 |
| 中文关键词: 急性肾损伤 肾小管 上皮细胞 miR-216a Kruppel样转录因子 9 核因子 -κB |
| 英文关键词: Acute kidney injury Kidney tubules Epithelial cells MiR-216a Kruppel-like factor 9 Nuclear transcrip-tion factor-κB |
| 基金项目: |
|
| 摘要点击次数: 1635 |
| 全文下载次数: 457 |
| 中文摘要: |
| 目的探讨 miR-216a对 Kruppel样转录因子 9(KLF9)的调控作用，及其对缺氧 -复氧( H/R)诱导的肾小管上皮细胞急性肾损伤的影响。方法将 293T细胞(人肾上皮细胞系)分为 KLF9野生型载体、 miR-216a mimics(类似物) +KLF9野生型载体、 miR-216a NC(阴性对照) +KLF9野生型载体，利用荧光素酶报告基因验证 miR-216a与 KLF9的结合关系。 H/R诱导大鼠肾脏近端肾小管上皮细胞，并转染 miR-216a mimics，将大鼠肾脏近端肾小管上皮细胞系 RPTC分为对照组， H/R组， H/R+miR-216a NC组， H/R+miR-216a mimics组。检测 miR-216a、KLF9、核因子 -κB(NF-κB)、肿瘤坏死因子 α(TNF-α)、血管生长因子 A(VEGF-A)、尿激酶型纤溶酶原激活物( uPA)mRNA表达。结果 miR-216a mimics+KLF9野生型共转染组的荧光素酶活性显著低于 KLF9野生型组、 miR-216a NC+KLF9野生型共转染组的荧光素酶活性(P＜0.05)。与对照组比较， H/R组和 H/R+miR-216a NC组 miR- 216a［(0.56±0.11)及( 0.48±0.06)比( 1.00±0.00)］表达量下调( P＜0.05)KLF9［(2.77±0.19)及( 2.79±0.10)比( 1.00±0.00)］NF-κB p65［(2.35±0.02)及(2.42±0.27)比(1.00±0.00)］、TNF-α［(2.40±0.21)及(，2.44±0.11)比( 1.00±0.00)］、 VEGF-A［( 4.17±0.0、7)及(4.19±0.11)比( 1.00±0.00)］、 uPA［(2.28±0.05)及( 2.38±0.13)比( 1.00±0.00)］mRNA表达量上调( P＜0.05)；与 H/R组和 H/R+ miR-216a NC组比较， H/R+miR-216a mimics组中 miR-216a［( 31.75±2.40)，F＝45.87，P＝0.000］表达量上调， KLF9［( 1.96±0.04)，F＝13.98，P＝0.005］、 NF-κB p65［(2.15±0.15)F＝14.89，P＝0.001］、 TNF-α［(1.79±0.10)，F＝18.90，P＝0.000］、 VEGF-A［(3.65±0.04)F＝15.94，P＝0.000］、 uPA［(2.06±0.11F＝14.22，P＝0.001］mRNA表达量下调(P＜0.05)。结论 miR-216a过)，表达通过靶向下，调 KLF9表达进而抑制 NF-κB信号通路，降，低肾小管上皮细胞急性肾损伤。 |
| 英文摘要: |
| Objective To explore the regulatory effect of miR-216a on Kruppel-like transcription factor 9(KLF9)and its effect on acute renal injury induced by hypoxia/reoxygenation(H/R)in renal tubular epithelial cells.Methods 293T cells were divided in- to KLF9 wild type vector，miR-216a mimics(analog)+ KLF9 wild type vector，mir-216a NC(negative control)+ KLF9 wild typevector.The binding relationship between miR-216a and KLF9 in 293T cells was detected by luciferase reporter gene.Rat proximalrenal tubular epithelial cell(PRTC)was induced by H/R and transfected by miR-216a mimics.RPTC was divided into control group，H/R group，H/R + miR-216a NC group and H/R + miR-216a mimicsgroup.The expressions of miR-216a，KLF9，nuclear tran- scription factor-κB(NF-κB)，tumor necrosis factor-alpha(TNF-α)，vascular growth factor A(VEGF-A)，urokinase-type plasmino- gen activator(uPA)were detected.Results The luciferase activity of miR-216a mimics+KLF9 wild-type co-transfection group wassignificantly lower than that of wild KLF9 group，wild KLF9 and miR-216a NC co-transfection group(P＜0.05).Compared with con- trol group，the expression levels of miR-216a［(0.56±0.11)and(0.48±0.06)vs.(1.00±0.00)］in the H/R group and H/R+miR-216a NC group were down-regulated(P＜0.05)，the expression of KLF9［( 2.77±0.19)and(2.79±0.10)vs.(1.00±0.00)］，NF-κB p65［(2.35±0.02)and(2.42±0.27)vs.(1.00±0.00)］，TNF-α［(2.40±0.21)and(2.44±0.11)vs.(1.00±0.00)］、 VEGF-A［(4.17±0.07)and(4.19±0.11)vs.(1.00±0.00)］，uPA［(2.28±0.05)and(2.38±0.13)vs.(1.00±0.00)］mRNA was up-regulated in H/R and H/R +miR -216a NC group(P＜0.05).Compared with H/R and H/R +miR-216a NC group，the expression of miR-216a［( 31.75±2.40)，F＝ 45.87，P＝0.000］was down-regulated(P＜0.05)the expression of KLF9［(1.96±0.04)F＝13.98，P＝0.005］NF-κB p65［(2.15± 0.15)， F＝14.89，P＝0.001］， TNF-α［( 1.79±0.10)，F＝18.90，P＝0.000］， VEGF-A［(，3.65±0.04)，F＝15.94，P，＝0.000］， uPA［(2.06±0.11)，F＝14.22，P＝0.001］mRNAwasdown-r，egulated in H/R +miR-216a mimics group(P＜0.05).Conclusion Overex-pression of miR-216a could inhibit NF-κB signaling pathway by targeting down-regulation of KLF9 expression and reduce acute re-nal injury in renal tubular epithelial cells. |
|
查看全文
查看/发表评论 下载PDF阅读器 |
| 关闭 |
