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Research Paper|Volume 14, Issue 5|pp 2210—2220

Circular RNA circ_0001006 aggravates cardiac hypertrophy via miR-214-3p/PAK6 axis

Xuefeng Lin1,2,3,4,5,6, Liqin Zhang6, Wei Zhang7, Xinjun Lei1, Qun Lu1, Aiqun Ma1,2,3,4
  • 1Department of Cardiovascular Medicine, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shanxi 710061, PR China
  • 2Key Laboratory of Molecular Cardiology, Xi’an Jiaotong University, Xi’an, Shanxi 710061, PR China
  • 3Institute of Cardiovascular Channelopathy, Xi’an Jiaotong University, Xi’an, Shanxi 7100161, PR China
  • 4Key Laboratory of Environment and Genes Related to Diseases, Xi’an Jiaotong University, Ministry of Education, Xi’an, Shanxi 7100161, PR China
  • 5Department of Cardiovascular Medicine, The First Affiliated Hospital of Baotou Medical College, Baotou, Inner Mongolia 014010, PR China
  • 6Baotou Medical College, Baotou, Inner Mongolia 014010, PR China
  • 7ECG Room, Xi’an Children’s Hospital, Xi’an, Shanxi 710061, PR China
Received: April 1, 2021Accepted: July 30, 2021Published: March 6, 2022
https://doi.org/10.18632/aging.203461

Copyright: © 2021 Lin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Aim: Circular RNAs (circRNAs) control gene expression in a series of physiological and pathological processes, but their role in heart disease is unknown. This research illustrates the role and potential mechanism of circRNA in cardiac hypertrophy.

Methods and Results: In this report, we found that circular RNA hsa_circ_0001006 (circ_0001006) was upregulated in cardiac hypertrophy mice and cardiomyocytes treated with angiotensin II (Ang II). Next, we noticed that gain of function circ_0001006 could induce cardiomyocyte hypertrophy; oppositely, knockdown of circ_0001006 remitted Ang II-induced cardiomyocyte hypertrophy. Biotin-coupled miRNA and RNA-pull down assays showed that miR-214-3p could bind with circ_0001006 and gain the function of miR-214-3p abrogated the pro-hypertrophy effect of circ_0001006. Furthermore, Further, dual-luciferase reporter assay showed that miR-214-3p could interact with 3′UTRs of the PAK6 gene, and circRNA_0001006 could block the above interactions. Additionally, PAK6 expression is inhibited by miR-214-3p mimic in cardiomyocytes but enhanced by over-expression of circRNA_000203 in vitro.

Conclusions: Our data demonstrated that circRNA_0001006 exacerbates cardiac hypertrophy via suppressing miR-214-3p leading to enhanced PAK6 levels.