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

DNMT3b 介导的 miR-181a-5p DNA 甲基化导致急性肾损伤引发肾间质纤维化

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作者: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

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 &

Conclusion

Hypermethylation of miR-181a-5p promoter mediated by DNMT3b promotes AKI induced RIF by targeting HDAC9 and SNAI2.

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.

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