DNA methylation of miR-181a-5p mediated by DNMT3b drives renal interstitial fibrosis developed from acute kidney injury

Huaxi Liu, Yijian Deng, Guanfeng Luo, Ying Yang, Bei Xie, Huiling Diao, Meilin Chen, Liqian Chen, Penghui Xie, Hiu Yee Kwan, Xiaoshan Zhao*, Xiaomin Sun*

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review

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.

Original languageEnglish
Pages (from-to)945-960
Number of pages16
JournalEpigenomics
Volume16
Issue number13
Early online date18 Jul 2024
DOIs
Publication statusPublished - Sept 2024

Scopus Subject Areas

  • Genetics
  • Cancer Research

User-Defined Keywords

  • acute kidney injury
  • DNMT3b
  • HDAC9
  • miR-181a-5p
  • renal interstitial fibrosis
  • SNAI2

Fingerprint

Dive into the research topics of 'DNA methylation of miR-181a-5p mediated by DNMT3b drives renal interstitial fibrosis developed from acute kidney injury'. Together they form a unique fingerprint.

Cite this