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In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge
Published on: June 15, 2018
MicroRNA-24 regulates cardiac fibrosis after myocardial infarction
Jue Wang1, Weicong Huang, Ruixia Xu
1State Key Laboratory of Translational Cardiovascular Medicine, Fuwai Hospital & Cardiovascular Institute, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Abstract:
Cardiac fibrosis after myocardial infarction (MI) has been identified as a key factor in the development of heart failure. Although dysregulation of microRNA (miRNA) is involved in various pathophysiological processes in the heart, the role of miRNA in fibrosis regulation after MI is not clear. Previously we observed the correlation between fibrosis and the miR-24 expression in hypertrophic hearts, herein we assessed how miR-24 regulates fibrosis after MI. Using qRT-PCR, we showed that miR-24 was down-regulated in the MI heart; the change in miR-24 expression was closely related to extracellular matrix (ECM) remodelling. In vivo, miR-24 could improve heart function and attenuate fibrosis in the infarct border zone of the heart two weeks after MI through intramyocardial injection of Lentiviruses. Moreover, in vitro experiments suggested that up-regulation of miR-24 by synthetic miR-24 precursors could reduce fibrosis and also decrease the differentiation and migration of cardiac fibroblasts (CFs). TGF-β (a pathological mediator of fibrotic disease) increased miR-24 expression, overexpression of miR-24 reduced TGF-β secretion and Smad2/3 phosphorylation in CFs. By performing microarray analyses and bioinformatics analyses, we found furin to be a potential target for miR-24 in fibrosis (furin is a protease which controls latent TGF-β activation processing). Finally, we demonstrated that protein and mRNA levels of furin were regulated by miR-24 in CFs. These findings suggest that miR-24 has a critical role in CF function and cardiac fibrosis after MI through a furin-TGF-β pathway. Thus, miR-24 may be used as a target for treatment of MI and other fibrotic heart diseases.
Insights
MicroRNA-24 (miR-24) is crucial for regulating cardiac fibrosis after myocardial infarction (MI). Restoring miR-24 levels improves heart function and reduces fibrosis by targeting furin and the TGF-β pathway.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Fibrosis Research
Background:
- Cardiac fibrosis post-myocardial infarction (MI) contributes to heart failure.
- MicroRNA (miRNA) dysregulation is implicated in cardiac pathophysiology, but their role in post-MI fibrosis remains unclear.
- Previous observations linked fibrosis and miR-24 in hypertrophic hearts.
Purpose of the Study:
- To investigate the regulatory role of miR-24 in cardiac fibrosis following MI.
- To elucidate the molecular mechanisms by which miR-24 influences cardiac fibroblast function and extracellular matrix remodeling.
Main Methods:
- Quantitative reverse transcription polymerase chain reaction (qRT-PCR) to assess miR-24 expression.
- In vivo studies using lentiviral delivery of miR-24 in a mouse MI model.
- In vitro experiments with synthetic miR-24 precursors and cardiac fibroblasts (CFs).
- Microarray and bioinformatics analyses to identify miR-24 targets.
- Western blotting to analyze protein levels and phosphorylation.
Main Results:
- miR-24 was downregulated in the MI heart, correlating with extracellular matrix (ECM) remodeling.
- Intramyocardial miR-24 delivery improved cardiac function and reduced fibrosis in vivo.
- Overexpression of miR-24 in CFs decreased fibrosis, differentiation, and migration.
- miR-24 inhibited TGF-β secretion and Smad2/3 phosphorylation in CFs.
- Furin was identified as a direct target of miR-24, with miR-24 regulating furin expression.
Conclusions:
- miR-24 plays a critical role in regulating cardiac fibroblast function and cardiac fibrosis after MI.
- The miR-24-furin-TGF-β pathway is a key mechanism in post-MI cardiac fibrosis.
- miR-24 represents a potential therapeutic target for MI and other fibrotic heart diseases.
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