首页|tRF-1:30对高糖诱导的肾小管上皮细胞炎性因子表达的影响

tRF-1:30对高糖诱导的肾小管上皮细胞炎性因子表达的影响

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目的 探讨tRF-1:30(tRF-1:30-Gln-CTG-4)对高糖(HG)诱导的肾小管上皮细胞(RTECs)中炎性因子表达的影响及分子机制.方法 将小鼠RTECs分为Control组、HG组、HG+tRF-1:30 mimic组、HG+tRF-1:30 NC组、HG+si-IKZF2组(IKAROS家族锌指2,tRF-1:30抑制剂)、HG+si-NC组.实时荧光定量PCR检测tRF-1:30、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、单核细胞趋化蛋白-1(MCP-1)和IKZF2 mRNA的水平.酶联免疫吸附试验检测炎性因子水平,Western blot检测IKZF2蛋白表达水平,双萤光素酶报告实验验证tRF-1:30和IKZF2的关系.结果 在HG诱导的RTECs中炎性因子的表达水平显著升高,而tRF-1:30表达水平显著降低.过表达tRF-1:30显著降低HG诱导的RTECs中炎性因子的表达水平.IKZF2在HG诱导的RTECs中显著高表达,进一步敲低IKZF2可抑制炎性因子的释放,而过表达tRF-1:30后IKZF2的表达水平下调.双萤光素酶报告实验进一步验证tRF-1:30与IKZF2可能存在靶向关系.结论 过表达tRF-1:30可能通过负向调控IKZF2的表达进而抑制HG诱导的RTECs炎性因子的释放.
Effect of tRF-1:30 on the expression of inflammatory factors in renal tubular epithelial cells induced by high glucose
Objective To investigate the effect and molecular mechanism of tRF-1:30-Gln-CTG-4(tRF-1:30)on the expression of inflammatory factors in high glucose(HG)-induced renal tubular epithelial cells(RTECs).Methods RTECs were divided into the control group,the HG group,the HG+tRF-1:30 mimic group,the HG+tRF-1:30 negative control(NC)group,the HG+si-IKZF2 group and the HG+si-NC group.Real-time quantitative polymerase chain reaction(RT-qPCR)was used to detect the expression levels of tRF-1:30,tumor necrosis factor-α(TNF-α),interleukin-6(IL-6),monocyte chemoattractant protein-1(MCP-1)and IKAROS family zinc finger protein 2(IKZF2).Enzyme-linked immunosorbent assay(ELISA)was used to detect levels of TNF-α,IL-6 and MCP-1.Protein expression of IKZF2 was detected by Western blot assay.Dual-luciferase reporter assay was used to detect the targeting relationship between tRF-1:30 and IKZF2.Results The expression levels of inflammatory factors were elevated in HG-induced RTECs,and the expression level of tRF-1:30 was decreased(P＜0.05).Overexpression of tRF-1:30 significantly decreased expression levels of inflammatory factors in HG-induced RTECs(P＜0.05),and the expression level of IKZF2 was significantly increased(P＜0.05).Further knockdown of IKZF2 can inhibit the release of inflammatory factors,and the expression level of IKZF2 was down-regulated after overexpression of tRF-1:30.Double luciferase reporting experiment further verified the possible targeting relationship between tRF-1:30 and IKZF2.Conclusion Overexpression of tRF-1:30 inhibits the expression of inflammatory factors in HG-induced RTECs by target binding and negatively regulating the expression of IKZF2.

diabetic nephropathiestelomeric repeat binding protein 1tRF-1:30-Gln-CTG-4renal tubular epithelial cellsinflammatory factorsIKAROS family zinc finger protein 2

夏雨薇、乔云阳、刘雪薇、施会敏、曲高婷、张爱青、甘卫华

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南京医科大学第二附属医院儿科(邮编 210003)

南京医科大学第四附属医院儿科

糖尿病肾病 端粒重复序列结合蛋白质1 tRF-1:30-Gln-CTG-4 肾小管上皮细胞 炎性因子 IKAROS家族锌指2

江苏省医学会儿科医学科研专项江苏省医学会儿科医学科研专项南京市卫生科技发展专项南京市卫生科技发展专项南京市卫生科技发展专项

SYH-32034-0073SYH-32034-0085YKK23209YKK23288YKK23289

2024

10.11958/20240046

天津医药
天津市医学科学技术信息研究所

天津医药

CSTPCD
影响因子：1.107
ISSN：0253-9896
年,卷(期)：2024.52(6)