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CARDIOLOGY / EXPERIMENTAL RESEARCH
MicroRNA-26b inhibits cardiac remodeling after myocardial infarction by targeting ring finger protein 6 expression
1
Department of Pharmacy, Nanchong Central Hospital, The Second Clinical Medical College, North Sichuan Medical College (University), Nanchong, Sichuan, China
2
Nanchong Key Laboratory of Individualized Drug Therapy, Nanchong, Sichuan, China
3
Cardiovascular Medicine, Nanchong Central Hospital, The Second Clinical Medical College, North Sichuan Medical College (University), Nanchong, Sichuan, China
Submission date: 2020-05-26
Final revision date: 2020-10-09
Acceptance date: 2020-11-19
Online publication date: 2021-04-17
Corresponding author
Tao Liu
Nanchong Central Hospital, The Second Clinical Medical College, North Sichuan Medical College (University), China
Nanchong Central Hospital, The Second Clinical Medical College, North Sichuan Medical College (University), China
Arch Med Sci 2024;20(6):2009-2021
KEYWORDS
TOPICS
ABSTRACT
Introduction:
This study aimed to determine the regulatory mechanism of miR-26b in myocardial infarction (MI)-induced cardiac remodeling through apoptosis.
Material and methods:
An MI rat model was established by left coronary artery ligation. Microarray data were analyzed to distinguish differentially expressed genes in MI. miR-26b was found to be poorly expressed, whereas ring finger protein 6 (RNF6) was highly expressed in MI. Consequently, miR-26b was identified to target RNF6 using dual-luciferase reporter assay and bioinformatics prediction. Furthermore, rats injected with a lentiviral vector expressing miR-26b mimic and/or RNF6 were used to evaluate the role of miR-26b and RNF6 in regulating cardiac function, infarct size, and cardiomyocyte apoptosis.
Results:
miR-26b overexpression improved cardiac function and increased left ventricular end-diastolic and end-systolic diameters. Meanwhile, increased miR-26b expression decreased infarct size and cardiomyocyte apoptosis. Moreover, RNF6 overexpression counteracted the role of miR-26b in cardiac function. Additionally, an in vitro cell model illustrated that miR-26b upregulation could increase cell viability and reduce apoptosis, whereas RNF6 overexpression reversed its effect. We also found that the miR-26b mimic could negatively modulate RNF6 expression to inactivate the ERα/Bcl-xL axis.
Conclusions:
miR-26b plays a protective role against cardiac remodeling after MI through inactivation of the RNF6/ERα/Bcl-xL axis, supporting miR-26b and RNF6 as potential therapeutic targets for MI.
This study aimed to determine the regulatory mechanism of miR-26b in myocardial infarction (MI)-induced cardiac remodeling through apoptosis.
Material and methods:
An MI rat model was established by left coronary artery ligation. Microarray data were analyzed to distinguish differentially expressed genes in MI. miR-26b was found to be poorly expressed, whereas ring finger protein 6 (RNF6) was highly expressed in MI. Consequently, miR-26b was identified to target RNF6 using dual-luciferase reporter assay and bioinformatics prediction. Furthermore, rats injected with a lentiviral vector expressing miR-26b mimic and/or RNF6 were used to evaluate the role of miR-26b and RNF6 in regulating cardiac function, infarct size, and cardiomyocyte apoptosis.
Results:
miR-26b overexpression improved cardiac function and increased left ventricular end-diastolic and end-systolic diameters. Meanwhile, increased miR-26b expression decreased infarct size and cardiomyocyte apoptosis. Moreover, RNF6 overexpression counteracted the role of miR-26b in cardiac function. Additionally, an in vitro cell model illustrated that miR-26b upregulation could increase cell viability and reduce apoptosis, whereas RNF6 overexpression reversed its effect. We also found that the miR-26b mimic could negatively modulate RNF6 expression to inactivate the ERα/Bcl-xL axis.
Conclusions:
miR-26b plays a protective role against cardiac remodeling after MI through inactivation of the RNF6/ERα/Bcl-xL axis, supporting miR-26b and RNF6 as potential therapeutic targets for MI.
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