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

doi:10.1080/17501911.2024.2370229

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 journal › Journal article › peer-review

3 Citations (Scopus)

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 language	English
Pages (from-to)	945-960
Number of pages	16
Journal	Epigenomics
Volume	16
Issue number	13
Early online date	18 Jul 2024
DOIs	https://doi.org/10.1080/17501911.2024.2370229
Publication status	Published - Sept 2024

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This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

User-Defined Keywords

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

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10.1080/17501911.2024.2370229

Cite this

@article{3ed85e444a3443b0ad651b7d4596c9f4,

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

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{\textquoteright}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.",

keywords = "acute kidney injury, DNMT3b, HDAC9, miR-181a-5p, renal interstitial fibrosis, SNAI2",

author = "Huaxi Liu and Yijian Deng and Guanfeng Luo and Ying Yang and Bei Xie and Huiling Diao and Meilin Chen and Liqian Chen and Penghui Xie and Kwan, \{Hiu Yee\} and Xiaoshan Zhao and Xiaomin Sun",

note = "This work was supported by the National Natural Science Foundation of China (81973666, 82274510), the Natural Science Foundation of Guangdong Province, China (2019A1515010816), the open project of state key laboratory of dampness syndrome of chinese medicine and the second affiliated hospital of guangzhou university of chinese medicine (sz2021kf12). Publisher Copyright: {\textcopyright} 2024 The Author(s). Published by Informa UK Limited, trading as Taylor \& Francis Group.",

year = "2024",

month = sep,

doi = "10.1080/17501911.2024.2370229",

language = "English",

volume = "16",

pages = "945--960",

journal = "Epigenomics",

issn = "1750-1911",

publisher = "Taylor and Francis Ltd.",

number = "13",

}

TY - JOUR

T1 - DNA methylation of miR-181a-5p mediated by DNMT3b drives renal interstitial fibrosis developed from acute kidney injury

AU - Liu, Huaxi

AU - Deng, Yijian

AU - Luo, Guanfeng

AU - Yang, Ying

AU - Xie, Bei

AU - Diao, Huiling

AU - Chen, Meilin

AU - Chen, Liqian

AU - Xie, Penghui

AU - Kwan, Hiu Yee

AU - Zhao, Xiaoshan

AU - Sun, Xiaomin

N1 - This work was supported by the National Natural Science Foundation of China (81973666, 82274510), the Natural Science Foundation of Guangdong Province, China (2019A1515010816), the open project of state key laboratory of dampness syndrome of chinese medicine and the second affiliated hospital of guangzhou university of chinese medicine (sz2021kf12). Publisher Copyright: © 2024 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

PY - 2024/9

Y1 - 2024/9

N2 - 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.

AB - 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.

KW - acute kidney injury

KW - DNMT3b

KW - HDAC9

KW - miR-181a-5p

KW - renal interstitial fibrosis

KW - SNAI2

UR - https://www.scopus.com/pages/publications/85198716524

U2 - 10.1080/17501911.2024.2370229

DO - 10.1080/17501911.2024.2370229

M3 - Journal article

AN - SCOPUS:85198716524

SN - 1750-1911

VL - 16

SP - 945

EP - 960

JO - Epigenomics

JF - Epigenomics

IS - 13

ER -

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

Abstract

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