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In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge
Published on: June 15, 2018
MicroRNA-26b inhibits cardiac remodeling after myocardial infarction by targeting ring finger protein 6 expression
Chun-Mei Tang1,2, Qiang Su1,2, Hai-Xia Zhao1,2
1Department of Pharmacy, Nanchong Central Hospital, The Second Clinical Medical College, North Sichuan Medical College (University), Nanchong, Sichuan, China.
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.
Insights
MicroRNA-26b (miR-26b) protects against heart damage after myocardial infarction (MI) by regulating ring finger protein 6 (RNF6). Upregulating miR-26b and targeting RNF6 show therapeutic potential for MI.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Gene Regulation
Background:
- Myocardial infarction (MI) triggers cardiac remodeling, a process involving cardiomyocyte apoptosis.
- Understanding the molecular mechanisms underlying MI-induced cardiac remodeling is crucial for developing effective therapies.
Purpose of the Study:
- To elucidate the regulatory role of microRNA-26b (miR-26b) in myocardial infarction (MI)-induced cardiac remodeling.
- To investigate the interaction between miR-26b and ring finger protein 6 (RNF6) in the context of cardiac injury.
Main Methods:
- Established a rat model of MI via left coronary artery ligation.
- Utilized microarray analysis to identify differentially expressed genes.
- Employed dual-luciferase reporter assays and bioinformatics to confirm miR-26b targeting of RNF6.
- Administered lentiviral vectors for miR-26b mimic and/or RNF6 overexpression in vivo and in vitro.
Main Results:
- miR-26b was downregulated, while RNF6 was upregulated in MI.
- Overexpression of miR-26b improved cardiac function, reduced infarct size, and decreased cardiomyocyte apoptosis.
- RNF6 overexpression counteracted the protective effects of miR-26b.
- miR-26b inactivated the RNF6/ERα/Bcl-xL signaling axis.
Conclusions:
- miR-26b exerts a protective effect against cardiac remodeling post-MI by downregulating RNF6.
- The miR-26b/RNF6/ERα/Bcl-xL pathway represents a potential therapeutic target for MI treatment.
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