Position-specific oxidation of miR-1 encodes cardiac hypertrophy

Heeyoung Seok, Haejeong Lee, Sohyun Lee, Seung Hyun Ahn, Hye Sook Lee, Geun Woo D. Kim, Jongjin Peak, Jongyeun Park, You Kyung Cho, Yeojin Jeong, Dowoon Gu, Yeahji Jeong, Sangkyeong Eom, Eun Sook Jang, Sung Wook Chi

Research output: Contribution to journalArticlepeer-review

60 Citations (Scopus)


In pathophysiology, reactive oxygen species oxidize biomolecules that contribute to disease phenotypes1. One such modification, 8-oxoguanine2 (o8G), is abundant in RNA3 but its epitranscriptional role has not been investigated for microRNAs (miRNAs). Here we specifically sequence oxidized miRNAs in a rat model of the redox-associated condition cardiac hypertrophy4. We find that position-specific o8G modifications are generated in seed regions (positions 2–8) of selective miRNAs, and function to regulate other mRNAs through o8G•A base pairing. o8G is induced predominantly at position 7 of miR-1 (7o8G-miR-1) by treatment with an adrenergic agonist. Introducing 7o8G-miR-1 or 7U-miR-1 (in which G at position 7 is substituted with U) alone is sufficient to cause cardiac hypertrophy in mice, and the mRNA targets of o8G-miR-1 function in affected phenotypes; the specific inhibition of 7o8G-miR-1 in mouse cardiomyocytes was found to attenuate cardiac hypertrophy. o8G-miR-1 is also implicated in patients with cardiomyopathy. Our findings show that the position-specific oxidation of miRNAs could serve as an epitranscriptional mechanism to coordinate pathophysiological redox-mediated gene expression.

Original languageEnglish
Pages (from-to)279-285
Number of pages7
Issue number7820
Publication statusPublished - 2020 Aug 13

ASJC Scopus subject areas

  • General


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