Circ_nuclear factor I X (circNfix) attenuates pressure overload-induced cardiac hypertrophy via regulating miR-145-5p/ATF3 axis
Cardiac hypertrophy can cause heart failure. However, the mechanisms underlying the progression of cardiac hypertrophy remain unclear. Emerging evidence suggests that circular RNAs (circRNAs) play a critical role in cardiac hypertrophy. However, the association between circ_nuclear factor I X (circN...
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doaj-cc19272e079341ab9b971ea311124fb02021-09-06T14:06:26ZengTaylor & Francis GroupBioengineered2165-59792165-59872021-01-011215373538510.1080/21655979.2021.19604621960462Circ_nuclear factor I X (circNfix) attenuates pressure overload-induced cardiac hypertrophy via regulating miR-145-5p/ATF3 axisJun Pan0Zhenjun Xu1Guanjun Guo2Can Xu3Zhizhao Song4Kunsheng Li5Kai Zhong6Dongjin Wang7The Affiliated Drum Tower Hospital of Nanjing University Medical SchoolThe Affiliated Drum Tower Hospital of Nanjing University Medical SchoolThe Affiliated Drum Tower Hospital of Nanjing University Medical SchoolThe Affiliated Drum Tower Hospital of Nanjing University Medical SchoolThe Affiliated Drum Tower Hospital of Nanjing University Medical SchoolThe Affiliated Drum Tower Hospital of Nanjing University Medical SchoolThe Affiliated Drum Tower Hospital of Nanjing University Medical SchoolThe Affiliated Drum Tower Hospital of Nanjing University Medical SchoolCardiac hypertrophy can cause heart failure. However, the mechanisms underlying the progression of cardiac hypertrophy remain unclear. Emerging evidence suggests that circular RNAs (circRNAs) play a critical role in cardiac hypertrophy. However, the association between circ_nuclear factor I X (circNfix) and cardiac hypertrophy remain largely unknown. Therefore, the aim of the present study was to explore the role of circNfix in cardiac hypertrophy. In order to detect the function of circNfix in cardiac hypertrophy, cardiomyocytes were stimulated with angiotensin II (Ang II) to mimic the pathogenesis of the disease. In addition, pressure overload-induced cardiac hypertrophy in a mouse model was established using transverse aortic constriction (TAC) surgery. The mechanism via which circNfix regulated cardiac hypertrophy was investigated using RNA pull-down and luciferase reporter assays, and fluorescence in situ hybridization (FISH). circNfix was downregulated in Ang II-treated cardiomyocytes. Similarly, circNfix expression was markedly downregulated in mice following TAC surgery. In addition, circNfix overexpression significantly prevented the progression of cardiac hypertrophy in TAC-treated mice. Luciferase activity and RNA pull-down assays indicated that circNfix could indirectly target activating transcription factor 3 (ATF3) by binding with microRNA (miR)-145-5p in cardiomyocytes. miR-145-5p overexpression or ATF3 knockdown could reverse the effects of circNfix in Ang II-treated mouse cardiomyocytes. circNfix attenuated pressure overload-induced cardiac hypertrophy by regulating the miR-145-5p/ATF3 axis. Therefore, circNfix may serve as a molecular target for cardiac hypertrophy treatment.http://dx.doi.org/10.1080/21655979.2021.1960462hypertrophycircrnamirnaatf3nfixcircnfix |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Jun Pan Zhenjun Xu Guanjun Guo Can Xu Zhizhao Song Kunsheng Li Kai Zhong Dongjin Wang |
spellingShingle |
Jun Pan Zhenjun Xu Guanjun Guo Can Xu Zhizhao Song Kunsheng Li Kai Zhong Dongjin Wang Circ_nuclear factor I X (circNfix) attenuates pressure overload-induced cardiac hypertrophy via regulating miR-145-5p/ATF3 axis Bioengineered hypertrophy circrna mirna atf3 nfix circnfix |
author_facet |
Jun Pan Zhenjun Xu Guanjun Guo Can Xu Zhizhao Song Kunsheng Li Kai Zhong Dongjin Wang |
author_sort |
Jun Pan |
title |
Circ_nuclear factor I X (circNfix) attenuates pressure overload-induced cardiac hypertrophy via regulating miR-145-5p/ATF3 axis |
title_short |
Circ_nuclear factor I X (circNfix) attenuates pressure overload-induced cardiac hypertrophy via regulating miR-145-5p/ATF3 axis |
title_full |
Circ_nuclear factor I X (circNfix) attenuates pressure overload-induced cardiac hypertrophy via regulating miR-145-5p/ATF3 axis |
title_fullStr |
Circ_nuclear factor I X (circNfix) attenuates pressure overload-induced cardiac hypertrophy via regulating miR-145-5p/ATF3 axis |
title_full_unstemmed |
Circ_nuclear factor I X (circNfix) attenuates pressure overload-induced cardiac hypertrophy via regulating miR-145-5p/ATF3 axis |
title_sort |
circ_nuclear factor i x (circnfix) attenuates pressure overload-induced cardiac hypertrophy via regulating mir-145-5p/atf3 axis |
publisher |
Taylor & Francis Group |
series |
Bioengineered |
issn |
2165-5979 2165-5987 |
publishDate |
2021-01-01 |
description |
Cardiac hypertrophy can cause heart failure. However, the mechanisms underlying the progression of cardiac hypertrophy remain unclear. Emerging evidence suggests that circular RNAs (circRNAs) play a critical role in cardiac hypertrophy. However, the association between circ_nuclear factor I X (circNfix) and cardiac hypertrophy remain largely unknown. Therefore, the aim of the present study was to explore the role of circNfix in cardiac hypertrophy. In order to detect the function of circNfix in cardiac hypertrophy, cardiomyocytes were stimulated with angiotensin II (Ang II) to mimic the pathogenesis of the disease. In addition, pressure overload-induced cardiac hypertrophy in a mouse model was established using transverse aortic constriction (TAC) surgery. The mechanism via which circNfix regulated cardiac hypertrophy was investigated using RNA pull-down and luciferase reporter assays, and fluorescence in situ hybridization (FISH). circNfix was downregulated in Ang II-treated cardiomyocytes. Similarly, circNfix expression was markedly downregulated in mice following TAC surgery. In addition, circNfix overexpression significantly prevented the progression of cardiac hypertrophy in TAC-treated mice. Luciferase activity and RNA pull-down assays indicated that circNfix could indirectly target activating transcription factor 3 (ATF3) by binding with microRNA (miR)-145-5p in cardiomyocytes. miR-145-5p overexpression or ATF3 knockdown could reverse the effects of circNfix in Ang II-treated mouse cardiomyocytes. circNfix attenuated pressure overload-induced cardiac hypertrophy by regulating the miR-145-5p/ATF3 axis. Therefore, circNfix may serve as a molecular target for cardiac hypertrophy treatment. |
topic |
hypertrophy circrna mirna atf3 nfix circnfix |
url |
http://dx.doi.org/10.1080/21655979.2021.1960462 |
work_keys_str_mv |
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1717779324712517632 |