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The role of lncRNAKCNQ1OT1/miR-301b/Tcf7 axis in cardiac hypertrophy

Published online by Cambridge University Press:  08 March 2024

Mingyao E Open the ORCID record for Mingyao E [Opens in a new window] ,
Feifei Ren ,
Yanhua Yu ,
Haiyan Li  and
Chao Shen
Mingyao E*
Affiliation:
Department of Pharmacology, Baicheng Medical College, Baicheng, China
Feifei Ren
Affiliation:
Nursing Department of Baicheng Hospital, Baicheng Medical College, Baicheng, China
Yanhua Yu
Affiliation:
Department of Pharmacology, Baicheng Medical College, Baicheng, China
Haiyan Li
Affiliation:
Department of Pharmacology, Baicheng Medical College, Baicheng, China
Chao Shen
Affiliation:
Department of Pharmacology, Baicheng Medical College, Baicheng, China
*
Corresponding author: Mingyao E, Email: emingyao202201@163.com
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Abstract

Objective:

Cardiac hypertrophy, acting as a pathologic process of chronic hypertension and coronary disease, and its underlying mechanisms still need to be explored. Long non-coding RNA (LncRNA) potassium voltage-gated channel subfamily Q member 1 Transcript 1 (KCNQ1OT1) has been implicated in myocardial infarction. However, its role in cardiac hypertrophy remains reported.

Method:

To explore the regulated effect of lncRNAKCNQ1OT1 and miR-301b in cardiac hypertrophy, gain-and-lose function assays were tested. The expression of lncRNAKCNQ1OT1 and miR-301b were tested by quantitative real time polymerase chain reaction (qRT-PCR). The levels of transcription factor 7 (Tcf7), Proto-oncogene c-myc (c-myc), Brainnatriureticpeptide (BNP) and β-myosin heavy chain (β-MHC) were detected by Western blot. Additionally, luciferase analysis revealed interaction between lncRNAKCNQ1OT1, BNPβ-MHCmiR-301b, and Tcf7.

Result:

LncRNAKCNQ1OT1 overexpression significantly induced cardiac hypertrophy. Furthermore, lncRNAKCNQ1OT1 acts as a sponge for microRNA-301b, which exhibited lower expression in cardiac hypertrophy model, indicating an anti-hypertrophic role. Furthermore, the BNP and β-MHC expression increased, as well as cardiomyocyte surface area, with Ang II treatment, while the effect was repealed by miR-301b. Moreover, the protein expression of Tcf7 was inversely regulated by miR-301b and Antisense miRNA oligonucleotides (AMO)-301b.

Conclusion:

Our study has shown that overexpression of lncRNAKCNQ1OT1 could promote the development of cardiac hypertrophy by regulating miR-301b and Tcf7. Therefore, inhibition of lncRNAKCNQ1OT1 might be a potential therapeutic strategy for cardiac hypertrophy.

Keywords

Cardiac hypertrophylncRNAKCNQ1OT1miR-301bTcf7c-myc
Type
Original Article
Information
Cardiology in the Young , First View , pp. 1 - 13
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Copyright
© The Author(s), 2024. Published by Cambridge University Press

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