PDF(Pubmed)
Abstract：
Aim: To explore the role of miR-181a-5p in the progression of acute kidney injury (AKI) to renal interstitial fibrosis (RIF) from the perspective of DNA methylation.Materials & methods: The role of miR-181a-5p was confirmed by collecting clinical samples, injecting miR-181a-5p agomir into tail vein, and transfecting miR-181a-5p mimic in vitro. The mechanism of miR-181a-5p\'s influence on AKI induced RIF was investigated by methylation-specific PCR, bioinformatic analysis, transcriptome sequencing and so on.Results: MiR-181a-5p plays an important role in AKI induced RIF. DNMT3b-mediated miR-181a-5p promoter hypermethylation is the main reason for the downregulation of miR-181a-5p. HDAC9 and SNAI2 are direct targets of miR-181a-5p.Conclusion: Hypermethylation of miR-181a-5p promoter mediated by DNMT3b promotes AKI induced RIF by targeting HDAC9 and SNAI2.
[Box: see text].
[Box: see text].
摘要：
目的:从DNA甲基化角度探讨miR-181a-5p在急性肾损伤(AKI)进展为肾间质纤维化(RIF)中的作用。材料与方法：通过收集临床样本证实miR-181a-5p的作用，将miR-181a-5p阿戈米尔注射到尾静脉，并体外转染miR-181a-5p模拟物。通过甲基化特异性PCR研究miR-181a-5p对AKI诱导的RIF的影响机制。生物信息学分析，转录组测序等。结果:MiR-181a-5p在AKI诱导的RIF中起重要作用。DNMT3b介导的miR-181a-5p启动子甲基化是miR-181a-5p下调的主要原因。HDAC9和SNAI2是miR-181a-5p的直接靶标。结论:DNMT3b介导的miR-181a-5p启动子超甲基化通过靶向HDAC9和SNAI2促进AKI诱导的RIF。
[方框：见正文]。
[方框：见正文]。
